dss  (Valiant)

 
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    Name:
    Dextran sulfate sodium salt
    Description:
    Dextran Sulfate Sodium Salt 8 000 avg Da M Wt
    Catalog Number:
    02101516-CF
    Price:
    None
    Category:
    Life Sciences Biochemicals Carbohydrates Polysaccharides
    Applications:
    Immunology, Antiviral, Antilipemic, Anticoagulant
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    Structured Review

    Valiant dss
    Depletion of macrophages reduces the severity of <t>DSS-induced</t> colitis promoted by <t>NaCl.</t> A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P
    Dextran Sulfate Sodium Salt 8 000 avg Da M Wt
    https://www.bioz.com/result/dss/product/Valiant
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dss - by Bioz Stars, 2021-07
    86/100 stars

    Images

    1) Product Images from "Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice"

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    Journal: World Journal of Gastroenterology

    doi: 10.3748/wjg.v24.i16.1779

    Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P
    Figure Legend Snippet: Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P

    Techniques Used: Mouse Assay, Activity Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

    NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry, Cell Culture, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry

    CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry, Isolation, Cell Culture, Enzyme-linked Immunosorbent Assay

    iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.
    Figure Legend Snippet: iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.

    Techniques Used: Mouse Assay, Injection, Staining, Confocal Microscopy, Fluorescence

    Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P
    Figure Legend Snippet: Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Staining

    2) Product Images from "Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity"

    Article Title: Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity

    Journal: Nature Communications

    doi: 10.1038/s41467-019-13883-y

    Commensal-specific antibody production is increased in Opg −/− mice. a , d Schematic cartoons depicting experimental designs. Commensal-specific fecal or serum immunoglobulins were detected by flow cytometry. b , c , e , f Feces and sera were collected from Opg −/− or co-housed WT mice at day 0 ( b , e ) or day 5 ( c , f ) after the onset of DSS consumption. Flow cytometry assays of DAPI-positive fecal bacteria bound by the indicated Igs were performed without ( b , c ) or with ( e , f ) serum. Representative data from two independent experiments are shown as the mean ± standard deviation. * p
    Figure Legend Snippet: Commensal-specific antibody production is increased in Opg −/− mice. a , d Schematic cartoons depicting experimental designs. Commensal-specific fecal or serum immunoglobulins were detected by flow cytometry. b , c , e , f Feces and sera were collected from Opg −/− or co-housed WT mice at day 0 ( b , e ) or day 5 ( c , f ) after the onset of DSS consumption. Flow cytometry assays of DAPI-positive fecal bacteria bound by the indicated Igs were performed without ( b , c ) or with ( e , f ) serum. Representative data from two independent experiments are shown as the mean ± standard deviation. * p

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry, Standard Deviation

    Absence of Opg ameliorates DSS-induced colitis. a Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b Colon length was measured after sacrifice at day 8. c Representative histology of hematoxylin- and eosin-stained colonic tissue from WT and Opg −/− mice with DSS-induced colitis on day 8. d Stool scores were measured as described in the Methods. e Spleen weight was measured after sacrifice at day 8. a , b , d , and e Data are presented as the mean ± SEM. ** p
    Figure Legend Snippet: Absence of Opg ameliorates DSS-induced colitis. a Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b Colon length was measured after sacrifice at day 8. c Representative histology of hematoxylin- and eosin-stained colonic tissue from WT and Opg −/− mice with DSS-induced colitis on day 8. d Stool scores were measured as described in the Methods. e Spleen weight was measured after sacrifice at day 8. a , b , d , and e Data are presented as the mean ± SEM. ** p

    Techniques Used: Staining, Mouse Assay

    Non-hematopoietic cells in Opg −/− mice contribute to relief of DSS colitis symptoms. a , e Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b , f Fecal clinical scores were measured as described in the Methods. c , g Colon length was measured after sacrifice at day 8. d , h Spleen weight was measured after sacrifice at day 8. WT or Opg −/− recipient mice following bone marrow transplantation from WT donors ( a – d ) and WT recipient mice following bone marrow transplantation from WT or Opg −/− donors ( e – h ) treated with 1.5% DSS for 7 days. Data are representative of two independent experiments. ** p
    Figure Legend Snippet: Non-hematopoietic cells in Opg −/− mice contribute to relief of DSS colitis symptoms. a , e Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b , f Fecal clinical scores were measured as described in the Methods. c , g Colon length was measured after sacrifice at day 8. d , h Spleen weight was measured after sacrifice at day 8. WT or Opg −/− recipient mice following bone marrow transplantation from WT donors ( a – d ) and WT recipient mice following bone marrow transplantation from WT or Opg −/− donors ( e – h ) treated with 1.5% DSS for 7 days. Data are representative of two independent experiments. ** p

    Techniques Used: Mouse Assay, Transplantation Assay

    3) Product Images from "Estrogen Receptor α Loss-of-Function Protects Female Mice From DSS-Induced Experimental Colitis"

    Article Title: Estrogen Receptor α Loss-of-Function Protects Female Mice From DSS-Induced Experimental Colitis

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2017.12.003

    DSS-induced colitis in WT, ERβ-KO, and ERα-KO male and female mice. Ten- to 12-week-old male (M) and female (F) WT, ERβ-KO, and ERα-KO mice were fed 2.5% DSS-supplemented drinking water for 5 days and killed on day 6. ( A ) Body weights were recorded at days 0, 5, and 6 and are expressed as the percentage of initial (day 0) weight. ( B ) The disease activity index (DAI) was calculated for each mouse at day 6 (encompassing body weight loss, stool consistency, and hemoccult scores). Analysis of variance (ANOVA) F = 36.3; P
    Figure Legend Snippet: DSS-induced colitis in WT, ERβ-KO, and ERα-KO male and female mice. Ten- to 12-week-old male (M) and female (F) WT, ERβ-KO, and ERα-KO mice were fed 2.5% DSS-supplemented drinking water for 5 days and killed on day 6. ( A ) Body weights were recorded at days 0, 5, and 6 and are expressed as the percentage of initial (day 0) weight. ( B ) The disease activity index (DAI) was calculated for each mouse at day 6 (encompassing body weight loss, stool consistency, and hemoccult scores). Analysis of variance (ANOVA) F = 36.3; P

    Techniques Used: Mouse Assay, Activity Assay

    Colon tissue gene expression of Socs3 , Ctsd , and Fos in DSS-treated ERα-KO mice and SOCS3 , CTSD , FOS , ERα , and ERβ in UC patients. Complementary DNA was prepared from ( A ) distal colon tissue from DSS-treated mice or non–DSS-treated controls or ( B–D ) colonic biopsy samples from UC patients or non–inflammatory bowel disease controls. Quantitative polymerase chain reaction was performed for ( A and B ) Socs3 , Ctsd , and Fos , ( C ) ERα , and ( D ) ERβ . Data are represented as the means ± SEM of n = 5–17 samples/group. * P ≤ .05, ** P ≤ .01, and *** P ≤ .001. Ctrl, control.
    Figure Legend Snippet: Colon tissue gene expression of Socs3 , Ctsd , and Fos in DSS-treated ERα-KO mice and SOCS3 , CTSD , FOS , ERα , and ERβ in UC patients. Complementary DNA was prepared from ( A ) distal colon tissue from DSS-treated mice or non–DSS-treated controls or ( B–D ) colonic biopsy samples from UC patients or non–inflammatory bowel disease controls. Quantitative polymerase chain reaction was performed for ( A and B ) Socs3 , Ctsd , and Fos , ( C ) ERα , and ( D ) ERβ . Data are represented as the means ± SEM of n = 5–17 samples/group. * P ≤ .05, ** P ≤ .01, and *** P ≤ .001. Ctrl, control.

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction

    4) Product Images from "Targeted 25-hydroxyvitamin D3 1α-hydroxylase Adoptive Gene Therapy Ameliorates DSS-induced Colitis Without Causing Hypercalcemia in Mice"

    Article Title: Targeted 25-hydroxyvitamin D3 1α-hydroxylase Adoptive Gene Therapy Ameliorates DSS-induced Colitis Without Causing Hypercalcemia in Mice

    Journal: Molecular Therapy

    doi: 10.1038/mt.2014.201

    Engraftment of CD11b + /Gr1 + monocytes at the inflamed colon of mice with dextran sulfate sodium (DSS)-induced colitis. ( a and b ) DSS colitis in 8-week-old C57BL/6 mice was induced as described in Materials and Methods. Gr1 + monocytes were isolated from
    Figure Legend Snippet: Engraftment of CD11b + /Gr1 + monocytes at the inflamed colon of mice with dextran sulfate sodium (DSS)-induced colitis. ( a and b ) DSS colitis in 8-week-old C57BL/6 mice was induced as described in Materials and Methods. Gr1 + monocytes were isolated from

    Techniques Used: Mouse Assay, Isolation

    5) Product Images from "IFN- γ drives inflammatory bowel disease pathogenesis through VE-cadherin–directed vascular barrier disruption"

    Article Title: IFN- γ drives inflammatory bowel disease pathogenesis through VE-cadherin–directed vascular barrier disruption

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI124884

    The intestinal vasculature is characterized by IFN-γ–mediated barrier dysfunction in murine DSS-induced colitis and human IBD. ( A – D ) Seventy-kDa FITC-dextran (10 mg/mL) was injected i.v. in mice with acute and chronic DSS-colitis. Accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of FITC signal inside the crypts over the total FITC signal. Vessel permeability was reduced in Ifngr2 ΔEC ( n = 4) ( A ) and Ifngr2 iΔEC ( n = 7) mice ( B ) compared with control mice ( n = 4 and 7, respectively) during acute ( A and B ) and chronic colitis ( C ; 4 Ifngr2 ΔEC vs. 5 control). For quantitative evaluation, 10–12 crypts were analyzed per mouse. Scale bars: 50 μm. ( D ) Control mice with αVEGF treatment (150 μg/mouse, n = 8) and Ifngr2 ΔEC mice ( n = 8) showed reduced vascular permeability in contrast to control mice treated with isotype antibody (150 μg/mouse, n = 7). Scale bar: 50 μm. For quantitative evaluation, 10 crypts per mouse were analyzed. Pooled results from 2 independent experiments are shown. ( E ) Human IBD patients with active disease ( n = 8) or remission ( n = 7) or control patients without IBD ( n = 3) underwent pCLE. Fluorescein accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of fluorescein signal inside the crypts over total fluorescein signal. Vessel permeability was increased in active disease (10 crypts per patient). Scale bar: 20 μm. Representative pictures are shown. Quantitative evaluations (right side of each panel) are shown as box-and-whisker plots (horizontal bars, median; box borders, 25th and 75th percentiles; whiskers, minimum and maximum values; A – D ) or means ± SD ( E ). Mann-Whitney U test ( A – C ), Kruskal-Wallis test followed by Dunn’s post hoc test ( D ), and 1-way ANOVA followed by Tukey’s post hoc test ( D ) were used to determine statistical significance (*** P
    Figure Legend Snippet: The intestinal vasculature is characterized by IFN-γ–mediated barrier dysfunction in murine DSS-induced colitis and human IBD. ( A – D ) Seventy-kDa FITC-dextran (10 mg/mL) was injected i.v. in mice with acute and chronic DSS-colitis. Accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of FITC signal inside the crypts over the total FITC signal. Vessel permeability was reduced in Ifngr2 ΔEC ( n = 4) ( A ) and Ifngr2 iΔEC ( n = 7) mice ( B ) compared with control mice ( n = 4 and 7, respectively) during acute ( A and B ) and chronic colitis ( C ; 4 Ifngr2 ΔEC vs. 5 control). For quantitative evaluation, 10–12 crypts were analyzed per mouse. Scale bars: 50 μm. ( D ) Control mice with αVEGF treatment (150 μg/mouse, n = 8) and Ifngr2 ΔEC mice ( n = 8) showed reduced vascular permeability in contrast to control mice treated with isotype antibody (150 μg/mouse, n = 7). Scale bar: 50 μm. For quantitative evaluation, 10 crypts per mouse were analyzed. Pooled results from 2 independent experiments are shown. ( E ) Human IBD patients with active disease ( n = 8) or remission ( n = 7) or control patients without IBD ( n = 3) underwent pCLE. Fluorescein accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of fluorescein signal inside the crypts over total fluorescein signal. Vessel permeability was increased in active disease (10 crypts per patient). Scale bar: 20 μm. Representative pictures are shown. Quantitative evaluations (right side of each panel) are shown as box-and-whisker plots (horizontal bars, median; box borders, 25th and 75th percentiles; whiskers, minimum and maximum values; A – D ) or means ± SD ( E ). Mann-Whitney U test ( A – C ), Kruskal-Wallis test followed by Dunn’s post hoc test ( D ), and 1-way ANOVA followed by Tukey’s post hoc test ( D ) were used to determine statistical significance (*** P

    Techniques Used: Injection, Mouse Assay, Permeability, Whisker Assay, MANN-WHITNEY

    Treatment with imatinib restores vascular barrier function and reduces DSS-induced inflammation. ( A ) Imatinib (0.01 μg/mL) reduced IFN-γ–induced (100 U/mL) endothelial cell (MIEC) permeability in vitro; values are normalized to untreated cells. ( B ) Immunofluorescence staining of VE-cadherin (green), counterstained by DRAQ5 (blue), in MIECs treated with IFN-γ (100 U/mL), imatinib (0.01 μg/mL) plus IFN-γ, or imatinib alone or left untreated. Arrows indicate linear VE-cadherin pattern at cell-cell contacts; asterisks mark internalization. Scale bar: 25 μm. ( C – F ) Control mice received imatinib ( n = 11) orally daily during the course of DSS-colitis or PBS only ( n = 10) and were compared with Ifngr2 ΔEC mice receiving the same treatment ( n = 3, imatinib; n = 4, PBS). ( C ) In vivo permeability of colonic vessels was assessed by i.v. injection of 70-kDa FITC-dextran (10 mg/mL). Accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of FITC signal inside the crypts over the total FITC signal in percent (10 crypts per mouse). Scale bar: 50 μm. Treatment with imatinib reduced the severity of DSS-colitis in control mice evaluated by endoscopy ( D ), colon length ( E ), and histologic examination by H E staining ( F ; scale bar: 100 μm). ( A and B ) One representative of 3 independent experiments is depicted. Quantitative evaluations are shown as box-and-whisker plots ( A and C ) (horizontal bars, median; box borders, 25th and 75th percentiles; whiskers, minimum and maximum values) or means ± SD ( D and E ). All graphs are means ± SD. One-way ANOVA followed by Tukey’s post hoc test ( A , D , and E ) and Kruskal-Wallis test followed by Dunn’s post hoc test ( C ) were used for statistical evaluation (* P
    Figure Legend Snippet: Treatment with imatinib restores vascular barrier function and reduces DSS-induced inflammation. ( A ) Imatinib (0.01 μg/mL) reduced IFN-γ–induced (100 U/mL) endothelial cell (MIEC) permeability in vitro; values are normalized to untreated cells. ( B ) Immunofluorescence staining of VE-cadherin (green), counterstained by DRAQ5 (blue), in MIECs treated with IFN-γ (100 U/mL), imatinib (0.01 μg/mL) plus IFN-γ, or imatinib alone or left untreated. Arrows indicate linear VE-cadherin pattern at cell-cell contacts; asterisks mark internalization. Scale bar: 25 μm. ( C – F ) Control mice received imatinib ( n = 11) orally daily during the course of DSS-colitis or PBS only ( n = 10) and were compared with Ifngr2 ΔEC mice receiving the same treatment ( n = 3, imatinib; n = 4, PBS). ( C ) In vivo permeability of colonic vessels was assessed by i.v. injection of 70-kDa FITC-dextran (10 mg/mL). Accumulation in intestinal crypts (arrows) indicates vessel permeability, calculated as the ratio of FITC signal inside the crypts over the total FITC signal in percent (10 crypts per mouse). Scale bar: 50 μm. Treatment with imatinib reduced the severity of DSS-colitis in control mice evaluated by endoscopy ( D ), colon length ( E ), and histologic examination by H E staining ( F ; scale bar: 100 μm). ( A and B ) One representative of 3 independent experiments is depicted. Quantitative evaluations are shown as box-and-whisker plots ( A and C ) (horizontal bars, median; box borders, 25th and 75th percentiles; whiskers, minimum and maximum values) or means ± SD ( D and E ). All graphs are means ± SD. One-way ANOVA followed by Tukey’s post hoc test ( A , D , and E ) and Kruskal-Wallis test followed by Dunn’s post hoc test ( C ) were used for statistical evaluation (* P

    Techniques Used: Permeability, In Vitro, Immunofluorescence, Staining, Mouse Assay, In Vivo, Injection, Whisker Assay

    6) Product Images from "Melatonin controls microbiota in colitis by goblet cell differentiation and antimicrobial peptide production through Toll-like receptor 4 signalling"

    Article Title: Melatonin controls microbiota in colitis by goblet cell differentiation and antimicrobial peptide production through Toll-like receptor 4 signalling

    Journal: Scientific Reports

    doi: 10.1038/s41598-020-59314-7

    Intraperitoneal administration of melatonin ameliorates DSS-induced colitis through TLR4 signal pathway. Wild type (WT) and TLR4 knockout (TLR4 KO) mice were administered 2.5% DSS in drinking water and treated i.p. with 0.25% EtOH/PBS (Veh) or melatonin (Mel, 10 mg/kg/day) from days 1 to 8. ( a , b ) Disease activity index (DAI). ( c , d ) Colon length. ( e–j ) Histopathology of colon. ( e , f ) Representative image of periodic acid-Schiff (PAS)-stain. ( g , h ) Histopathologic score. ( i , j ) Goblet cell score. Data represent mean ± S.E.M. (n = 10). Statistical significance was assessed using one-way ANOVA followed by Dunnett post-test compared to DSS + Veh. * P
    Figure Legend Snippet: Intraperitoneal administration of melatonin ameliorates DSS-induced colitis through TLR4 signal pathway. Wild type (WT) and TLR4 knockout (TLR4 KO) mice were administered 2.5% DSS in drinking water and treated i.p. with 0.25% EtOH/PBS (Veh) or melatonin (Mel, 10 mg/kg/day) from days 1 to 8. ( a , b ) Disease activity index (DAI). ( c , d ) Colon length. ( e–j ) Histopathology of colon. ( e , f ) Representative image of periodic acid-Schiff (PAS)-stain. ( g , h ) Histopathologic score. ( i , j ) Goblet cell score. Data represent mean ± S.E.M. (n = 10). Statistical significance was assessed using one-way ANOVA followed by Dunnett post-test compared to DSS + Veh. * P

    Techniques Used: Knock-Out, Mouse Assay, Activity Assay, Histopathology, Staining

    7) Product Images from "TSG-6 in extracellular vesicles from canine mesenchymal stem/stromal is a major factor in relieving DSS-induced colitis"

    Article Title: TSG-6 in extracellular vesicles from canine mesenchymal stem/stromal is a major factor in relieving DSS-induced colitis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0220756

    cASC-EV injection ameliorated DSS-induced colitis in mice. EVs (100 μg), TSG-6 depleted EVs (100 μg), control EVs (100 μg), or vehicle control were injected IP one day after mice were administered 3% DSS. On days 3 and 5, the mice in each group were re-injected with EVs (100 μg), TSG-6 depleted EVs (100 μg), control EVs (100 μg), or vehicle control (PBS). Mice were monitored for changes in (A) body weight, (B) DAIs, and (C) colon lengths. (D) H E staining of colon sections and histological scores are shown. Scale bars, 100 μm. The results are shown as mean ± standard deviation (n = 6–8 in each group, *P
    Figure Legend Snippet: cASC-EV injection ameliorated DSS-induced colitis in mice. EVs (100 μg), TSG-6 depleted EVs (100 μg), control EVs (100 μg), or vehicle control were injected IP one day after mice were administered 3% DSS. On days 3 and 5, the mice in each group were re-injected with EVs (100 μg), TSG-6 depleted EVs (100 μg), control EVs (100 μg), or vehicle control (PBS). Mice were monitored for changes in (A) body weight, (B) DAIs, and (C) colon lengths. (D) H E staining of colon sections and histological scores are shown. Scale bars, 100 μm. The results are shown as mean ± standard deviation (n = 6–8 in each group, *P

    Techniques Used: Injection, Mouse Assay, Staining, Standard Deviation

    8) Product Images from "EGFR in Tumor-Associated Myeloid Cells Promotes Development of Colorectal Cancer in Mice and Associates With Outcomes of Patients"

    Article Title: EGFR in Tumor-Associated Myeloid Cells Promotes Development of Colorectal Cancer in Mice and Associates With Outcomes of Patients

    Journal: Gastroenterology

    doi: 10.1053/j.gastro.2017.03.053

    EGFR signaling in myeloid cells promotes formation of colitis-associated and Apc Min -driven intestinal tumorigenesis. ( A ) Hematoxylin-eosin colon staining of AOM/DSS-treated mice. Arrowheads depict tumors. Scale bars 1 mm. ( B ) Immunofluorescence double staining of EGFR/CD64 on colorectal tumors. Arrowheads depict presence of EGFR + /CD64 + cells. Scale bars 50 μm. ( C ) Tumor penetrance in AOM/DSS-treated mice (ctrl [control], n = 10; Egfr wa2/wa2 , n = 5; Egfr f/f , n = 22; Egfr ΔIEC and Egfr ΔMYL , n = 15; Egfr ΔIEC/ΔMYL , n = 12). * P
    Figure Legend Snippet: EGFR signaling in myeloid cells promotes formation of colitis-associated and Apc Min -driven intestinal tumorigenesis. ( A ) Hematoxylin-eosin colon staining of AOM/DSS-treated mice. Arrowheads depict tumors. Scale bars 1 mm. ( B ) Immunofluorescence double staining of EGFR/CD64 on colorectal tumors. Arrowheads depict presence of EGFR + /CD64 + cells. Scale bars 50 μm. ( C ) Tumor penetrance in AOM/DSS-treated mice (ctrl [control], n = 10; Egfr wa2/wa2 , n = 5; Egfr f/f , n = 22; Egfr ΔIEC and Egfr ΔMYL , n = 15; Egfr ΔIEC/ΔMYL , n = 12). * P

    Techniques Used: Staining, Mouse Assay, Immunofluorescence, Double Staining

    9) Product Images from "Different Susceptibilities between Apoe- and Ldlr-Deficient Mice to Inflammation-Associated Colorectal Carcinogenesis"

    Article Title: Different Susceptibilities between Apoe- and Ldlr-Deficient Mice to Inflammation-Associated Colorectal Carcinogenesis

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms17111806

    The experimental protocol of ( a ) the Apoe -deficient and WT mice that received AOM and DSS (Experiment 1) and ( b ) the Ldlr -deficient and WT mice that received AOM and DSS (Experiment 2). i.p., intraperitoneal.
    Figure Legend Snippet: The experimental protocol of ( a ) the Apoe -deficient and WT mice that received AOM and DSS (Experiment 1) and ( b ) the Ldlr -deficient and WT mice that received AOM and DSS (Experiment 2). i.p., intraperitoneal.

    Techniques Used: Mouse Assay

    The mRNA expression of ( a ) Cox-2 ; ( b ) Nos2 ; ( c ) Tnf-α ; ( d ) Il-1β ; and ( e ) Il-6 in the colorectal mucosa of the Apoe -deficient, Ldlr -deficient, and their respective wild mice that received AOM and DSS. The mRNA levels of these molecules were measured by Real-Time Quantitative Polymerase Chain Resction. The expression of all five molecules was significantly higher in the Apoe -deficient mice than in the WT mice ( p
    Figure Legend Snippet: The mRNA expression of ( a ) Cox-2 ; ( b ) Nos2 ; ( c ) Tnf-α ; ( d ) Il-1β ; and ( e ) Il-6 in the colorectal mucosa of the Apoe -deficient, Ldlr -deficient, and their respective wild mice that received AOM and DSS. The mRNA levels of these molecules were measured by Real-Time Quantitative Polymerase Chain Resction. The expression of all five molecules was significantly higher in the Apoe -deficient mice than in the WT mice ( p

    Techniques Used: Expressing, Mouse Assay

    Histopathological analysis of induced colorectal adenocarcinomas. ( a ) Representative histopathology of colonic adenocarcinomas induced by azoxymethane (AOM) and dextran sodium sulfate (DSS). They were classified into three types of differentiation, well-differentiated (wel), moderately differentiated (mod), and poorly differentiated (por). Hematoxylin and eosin (H E) stain used. Bars are 100 µm in “wel”, 60 µm in “mod”, and 60 µm in “por”; ( b ) percentages of adenocarcinomas developed in the Apoe -deficient and wild (C57BL/6J) mice that received AOM and DSS; ( c ) percentage of adenocarcinomas developed in the Ldlr -deficient and wild (C57BL/6J) mice that received AOM and DSS.
    Figure Legend Snippet: Histopathological analysis of induced colorectal adenocarcinomas. ( a ) Representative histopathology of colonic adenocarcinomas induced by azoxymethane (AOM) and dextran sodium sulfate (DSS). They were classified into three types of differentiation, well-differentiated (wel), moderately differentiated (mod), and poorly differentiated (por). Hematoxylin and eosin (H E) stain used. Bars are 100 µm in “wel”, 60 µm in “mod”, and 60 µm in “por”; ( b ) percentages of adenocarcinomas developed in the Apoe -deficient and wild (C57BL/6J) mice that received AOM and DSS; ( c ) percentage of adenocarcinomas developed in the Ldlr -deficient and wild (C57BL/6J) mice that received AOM and DSS.

    Techniques Used: Histopathology, H&E Stain, Mouse Assay

    10) Product Images from "Collagen degradation and neutrophilic infiltration: a vicious circle in inflammatory bowel disease"

    Article Title: Collagen degradation and neutrophilic infiltration: a vicious circle in inflammatory bowel disease

    Journal: Gut

    doi: 10.1136/gutjnl-2012-303252

    Proteases in dextran sodium sulfate (DSS)-induced colitis. Intestinal prolyl endopeptidase (PE) activity (A) of huCXCR2 knock-in mice treated with 2-day cycles of DSS over time confirmed by immunoblot with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a loading control (B). Active and total matrix metalloproteinase 9 (MMP9) levels (C) were confirmed by zymography (D), and MMP8 levels (E) were confirmed by immunoblot with GAPDH as a loading control (F). All values are mean+SEM (n=3–8). *p
    Figure Legend Snippet: Proteases in dextran sodium sulfate (DSS)-induced colitis. Intestinal prolyl endopeptidase (PE) activity (A) of huCXCR2 knock-in mice treated with 2-day cycles of DSS over time confirmed by immunoblot with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a loading control (B). Active and total matrix metalloproteinase 9 (MMP9) levels (C) were confirmed by zymography (D), and MMP8 levels (E) were confirmed by immunoblot with GAPDH as a loading control (F). All values are mean+SEM (n=3–8). *p

    Techniques Used: Activity Assay, Knock-In, Mouse Assay, Zymography

    Proline–glycine–proline (PGP) neutralisation in dextran sodium sulfate (DSS)-induced colitis. The Disease Activity Index (A) and colonic length (B) of huCXCR2 knock-in mice treated with 1.5% (w/v) DSS for 5 days, and daily intravenous injections of arginine–threonine–arginine (RTR) with phosphate-buffered saline (PBS) as control, or PGP antibody with isotype antibody as control, and non-DSS controls. (C) Histopathological scoring and (D) representative images of H E-stained intestinal sections of all groups. (E) Representative images of neutrophil (LY-6B.2) immunohistochemistry on intestinal sections of DSS-treated animals treated with RTR, PBS, PGP antibody and isotype antibody. (F) Myeloperoxidase (MPO) levels in intestinal tissue homogenates of all groups as a measurement of neutrophil infiltration. Original magnifications ×200. All values are mean+SEM (n=8). Significance of differences determined by two-tailed Student t test: *p
    Figure Legend Snippet: Proline–glycine–proline (PGP) neutralisation in dextran sodium sulfate (DSS)-induced colitis. The Disease Activity Index (A) and colonic length (B) of huCXCR2 knock-in mice treated with 1.5% (w/v) DSS for 5 days, and daily intravenous injections of arginine–threonine–arginine (RTR) with phosphate-buffered saline (PBS) as control, or PGP antibody with isotype antibody as control, and non-DSS controls. (C) Histopathological scoring and (D) representative images of H E-stained intestinal sections of all groups. (E) Representative images of neutrophil (LY-6B.2) immunohistochemistry on intestinal sections of DSS-treated animals treated with RTR, PBS, PGP antibody and isotype antibody. (F) Myeloperoxidase (MPO) levels in intestinal tissue homogenates of all groups as a measurement of neutrophil infiltration. Original magnifications ×200. All values are mean+SEM (n=8). Significance of differences determined by two-tailed Student t test: *p

    Techniques Used: Activity Assay, Knock-In, Mouse Assay, Staining, Immunohistochemistry, Two Tailed Test

    Protease expression and proline–glycine–proline (PGP) levels in dextran sodium sulfate (DSS)-induced colitis. (A) Immunohistochemistry of intestinal matrix metalloproteinase 8 (MMP8), MMP9 and prolyl endopeptidase (PE) (and negative control) on consecutive intestinal sections of a DSS-treated huCXCR2 knock-in mouse. Original magnification ×400. Intestinal N-Ac-PGP (B) and PGP (C) levels in DSS-induced colitis, expressed as ng (N-Ac-)PGP/g intestinal tissue. All values are mean+SEM (n=3–8). No significant differences were detected, although there was a strong trend towards increased N-Ac-PGP levels at day 8 (versus day 0, p=0.09, unpaired t-test).
    Figure Legend Snippet: Protease expression and proline–glycine–proline (PGP) levels in dextran sodium sulfate (DSS)-induced colitis. (A) Immunohistochemistry of intestinal matrix metalloproteinase 8 (MMP8), MMP9 and prolyl endopeptidase (PE) (and negative control) on consecutive intestinal sections of a DSS-treated huCXCR2 knock-in mouse. Original magnification ×400. Intestinal N-Ac-PGP (B) and PGP (C) levels in DSS-induced colitis, expressed as ng (N-Ac-)PGP/g intestinal tissue. All values are mean+SEM (n=3–8). No significant differences were detected, although there was a strong trend towards increased N-Ac-PGP levels at day 8 (versus day 0, p=0.09, unpaired t-test).

    Techniques Used: Expressing, Immunohistochemistry, Negative Control, Knock-In

    11) Product Images from "Interleukin-11-expressing fibroblasts have a unique gene signature correlated with poor prognosis of colorectal cancer"

    Article Title: Interleukin-11-expressing fibroblasts have a unique gene signature correlated with poor prognosis of colorectal cancer

    Journal: Nature Communications

    doi: 10.1038/s41467-021-22450-3

    The MEK/ERK Pathway is involved in Il11 upregulation in DSS-induced colitis. a , b Wild-type mice were treated with DSS, without or with NAC ( a ) or Abx ( b ). Colon cells were prepared and stained with CellRox-green, and ROS accumulation was analyzed by flow cytometry. Left panels show representative histograms of ROS levels in colon cells. Right panels show percentages of CellRox-green + cells from an individual mouse. Results are mean ± SEM. n = 4 (untreated or NAC-treated) or 3 (untreated or Abx-treated) mice. c Wild-type mice were treated as in a . Colonic expression of 16S rRNA, Hmox1 , and Il11 mRNA was determined using qPCR. Results are mean ± SEM. n = 11 (untreated) or 9 (NAC-treated) mice; pooled data from three independent experiments. d Abx blocks Il11 mRNA upregulation in the colon in DSS-treated mice. Wild-type mice were untreated or treated with DSS in the absence or presence of Abx. On day 5 after DSS treatment, qPCR was performed to determine the expression of bacterial 16S rRNA and Il11 mRNA in the colon. Results are mean ± SEM. n = 8 (untreated), 3 (Abx-treated), 10 (DSS-treated), or 8 (DSS + Abx-treated) mice; pooled data from three independent experiments. e – g Trametinib inhibits ERK phosphorylation and Il11 mRNA expression in the colon in DSS-treated mice. Wild-type mice were treated with DSS in the absence or presence of trametinib injection (at –6 and –30 h), and then colon sections were prepared and stained with anti-pERK antibody ( e ). Scale bars, 100 μm. pERK + and DAPI + areas were calculated, and the ratios of pERK + /DAPI + areas (%) were plotted ( f ). Results are mean ± SEM. n = 7 (untreated) or 5 (Trametinib-treated) mice; pooled data from two independent experiments. Il11 mRNA expression was determined using qPCR ( g ). Results are mean ± SEM. n = 6 (untreated) or 7 (Trametinib-treated) mice; Pooled data from two independent experiments. h , i NAC inhibits ERK phosphorylation in the colon in DSS-treated mice. Wild-type mice were treated with DSS in the absence or presence of NAC in the drinking water for 5 days. Colon sections were stained with anti-pERK antibody ( h ). Scale bar, 100 μm. The ratios of pERK + /DAPI + areas (%) are plotted as in ( f ) ( i ). Results are mean ± SEM. n = 7 (untreated) or 8 (NAC-treated) mice; pooled data from two independent experiments. Statistical significance was determined using the unpaired two-tailed Student’s t -test ( c , f , i ), two-tailed Mann–Whitney U test ( g ), two-way ANOVA with Tukey’s multiple comparison test ( d ), or one-way ANOVA with Tukey’s multiple comparison test ( a , b ). Source data are provided as a Source Data file.
    Figure Legend Snippet: The MEK/ERK Pathway is involved in Il11 upregulation in DSS-induced colitis. a , b Wild-type mice were treated with DSS, without or with NAC ( a ) or Abx ( b ). Colon cells were prepared and stained with CellRox-green, and ROS accumulation was analyzed by flow cytometry. Left panels show representative histograms of ROS levels in colon cells. Right panels show percentages of CellRox-green + cells from an individual mouse. Results are mean ± SEM. n = 4 (untreated or NAC-treated) or 3 (untreated or Abx-treated) mice. c Wild-type mice were treated as in a . Colonic expression of 16S rRNA, Hmox1 , and Il11 mRNA was determined using qPCR. Results are mean ± SEM. n = 11 (untreated) or 9 (NAC-treated) mice; pooled data from three independent experiments. d Abx blocks Il11 mRNA upregulation in the colon in DSS-treated mice. Wild-type mice were untreated or treated with DSS in the absence or presence of Abx. On day 5 after DSS treatment, qPCR was performed to determine the expression of bacterial 16S rRNA and Il11 mRNA in the colon. Results are mean ± SEM. n = 8 (untreated), 3 (Abx-treated), 10 (DSS-treated), or 8 (DSS + Abx-treated) mice; pooled data from three independent experiments. e – g Trametinib inhibits ERK phosphorylation and Il11 mRNA expression in the colon in DSS-treated mice. Wild-type mice were treated with DSS in the absence or presence of trametinib injection (at –6 and –30 h), and then colon sections were prepared and stained with anti-pERK antibody ( e ). Scale bars, 100 μm. pERK + and DAPI + areas were calculated, and the ratios of pERK + /DAPI + areas (%) were plotted ( f ). Results are mean ± SEM. n = 7 (untreated) or 5 (Trametinib-treated) mice; pooled data from two independent experiments. Il11 mRNA expression was determined using qPCR ( g ). Results are mean ± SEM. n = 6 (untreated) or 7 (Trametinib-treated) mice; Pooled data from two independent experiments. h , i NAC inhibits ERK phosphorylation in the colon in DSS-treated mice. Wild-type mice were treated with DSS in the absence or presence of NAC in the drinking water for 5 days. Colon sections were stained with anti-pERK antibody ( h ). Scale bar, 100 μm. The ratios of pERK + /DAPI + areas (%) are plotted as in ( f ) ( i ). Results are mean ± SEM. n = 7 (untreated) or 8 (NAC-treated) mice; pooled data from two independent experiments. Statistical significance was determined using the unpaired two-tailed Student’s t -test ( c , f , i ), two-tailed Mann–Whitney U test ( g ), two-way ANOVA with Tukey’s multiple comparison test ( d ), or one-way ANOVA with Tukey’s multiple comparison test ( a , b ). Source data are provided as a Source Data file.

    Techniques Used: Mouse Assay, Staining, Flow Cytometry, Expressing, Real-time Polymerase Chain Reaction, Injection, Two Tailed Test, MANN-WHITNEY

    Blockade of the MEK/ERK Pathway reduces proliferation and induces apoptosis in Tumor Tissues of AOM/DSS-treated mice. a Schema of administration of various inhibitors in AOM/DSS-treated mice. b – f After induction of colorectal tumors, wild-type mice were not treated or treated with Ab x for 8 weeks ( b ), NAC for 4 weeks ( c ), or trametinib at −6 and −30 h ( d – f ) (before sacrifice). On day 98–105 after AOM injection, mRNA was extracted from tumor (T) and non-tumor tissues (N), and Il11 expression was determined by qPCR ( b – d ). Results are mean ± SEM. n = 9 (untreated), 8 (nontumor, Abx-treated), or 7 (nontumor, Abx-treated) mice; pooled data from two independent experiments ( b ). n = 13 (untreated) or 8 (NAC-treated) mice; pooled data from two independent experiments ( c ). n = 10 (nontumor, untreated), 11 (tumor, untreated), 9 (nontumor, trametinib-treated), or 10 (nontumor, trametinib-treated) mice; pooled data from four independent experiments ( d ). Colon tumor sections were stained with anti-Ki67 or anti-CC3 antibodies ( e ). Ki67 + area and total area were calculated and the percentages of Ki67 + area per area are expressed ( f ). n = 8 (untreated) or 7 (trametinib-treated) mice. Numbers of CC3 + cells were counted and the total area was calculated, and CC3 + cells per area are expressed as arbitrary units (a.u.) ( f ). n = 8 (untreated) or 6 (trametinib-treated) mice. Statistical significance was determined using the unpaired two-tailed Student’s t -test ( f ) and two-way ANOVA with Tukey’s multiple comparison test ( b – d ). Source data are provided as a Source Data file.
    Figure Legend Snippet: Blockade of the MEK/ERK Pathway reduces proliferation and induces apoptosis in Tumor Tissues of AOM/DSS-treated mice. a Schema of administration of various inhibitors in AOM/DSS-treated mice. b – f After induction of colorectal tumors, wild-type mice were not treated or treated with Ab x for 8 weeks ( b ), NAC for 4 weeks ( c ), or trametinib at −6 and −30 h ( d – f ) (before sacrifice). On day 98–105 after AOM injection, mRNA was extracted from tumor (T) and non-tumor tissues (N), and Il11 expression was determined by qPCR ( b – d ). Results are mean ± SEM. n = 9 (untreated), 8 (nontumor, Abx-treated), or 7 (nontumor, Abx-treated) mice; pooled data from two independent experiments ( b ). n = 13 (untreated) or 8 (NAC-treated) mice; pooled data from two independent experiments ( c ). n = 10 (nontumor, untreated), 11 (tumor, untreated), 9 (nontumor, trametinib-treated), or 10 (nontumor, trametinib-treated) mice; pooled data from four independent experiments ( d ). Colon tumor sections were stained with anti-Ki67 or anti-CC3 antibodies ( e ). Ki67 + area and total area were calculated and the percentages of Ki67 + area per area are expressed ( f ). n = 8 (untreated) or 7 (trametinib-treated) mice. Numbers of CC3 + cells were counted and the total area was calculated, and CC3 + cells per area are expressed as arbitrary units (a.u.) ( f ). n = 8 (untreated) or 6 (trametinib-treated) mice. Statistical significance was determined using the unpaired two-tailed Student’s t -test ( f ) and two-way ANOVA with Tukey’s multiple comparison test ( b – d ). Source data are provided as a Source Data file.

    Techniques Used: Mouse Assay, Injection, Expressing, Real-time Polymerase Chain Reaction, Staining, Two Tailed Test

    Characterization of IL-11 + cells in CAC using Il11-Egfp reporter mice. a Protocol for induction of AOM/DSS-induced CAC in mice. Il11-Egfp reporter mice were intraperitoneally injected with AOM on day 0, followed by repeated DSS administration. Colorectal cancer gradually develops ~30 days after AOM injection. Unless otherwise indicated, the following experiments used tumor and nontumor tissues collected on day 98–105 after AOM/DSS treatment. b Representative image of tumor and adjacent nontumor tissues in the mouse colon on day 77 after AOM injection. Colon sections were stained with hematoxylin eosin (H E) ( n = 20 mice). Scale bar, 200 μm. c mRNA samples from tumor and nontumor tissues were analyzed using qPCR to determine the expression levels of the indicated genes. Results are mean ± SEM ( n = 6 mice). Results are representative of two independent experiments. d – f From colonic tumor tissues of Il11-Egfp reporter mice, single-cell suspensions were prepared, and percentages of IL-11 + (EGFP + ) cells were determined. Representative flow cytometry images are shown ( d ). Results are mean ± SEM ( n = 7 mice). Cells were stained with the indicated antibodies, and marker expression on EGFP + cells was analyzed by flow cytometry. A representative dot plot from three independent experiments shows the percentages of EGFP + cells expressing each marker ( n = 5 mice except for CD34 where n = 4 mice) ( e ). Percentages of EGFP + cells among podoplanin + cells ( f ). Results are mean ± SEM ( n = 5 mice). g Nontumor and tumor tissue sections were stained with anti-GFP antibody ( n = 4 mice). Scale bars, 100 μm. h – l Tumor sections were stained with anti-GFP along with anti-IL-11 ( h ) ( n = 4 mice), anti-E-cadherin ( j ) ( n = 4 mice), or anti-Ki67 ( k ) and anti-podoplanin ( k ) antibodies ( n = 5 mice). The right-hand panels show enlarged images of white boxes from the left-hand panels. White arrowheads indicate EGFP + cells expressing the respective markers shown in red. IL-11 + and EGFP + cell numbers were calculated, and IL-11 + /EGFP + areas as percentages of the total area are shown ( i ). Ki67 + and EGFP + cell numbers were calculated, and are shown as percentages of the total area ( l ). Results are mean ± SEM ( n = 5 mice). Scale bars, 100 μm. Statistical significance was determined using the two-tailed unpaired Student’s t -test ( c , d ). Source data are provided as a Source Data file.
    Figure Legend Snippet: Characterization of IL-11 + cells in CAC using Il11-Egfp reporter mice. a Protocol for induction of AOM/DSS-induced CAC in mice. Il11-Egfp reporter mice were intraperitoneally injected with AOM on day 0, followed by repeated DSS administration. Colorectal cancer gradually develops ~30 days after AOM injection. Unless otherwise indicated, the following experiments used tumor and nontumor tissues collected on day 98–105 after AOM/DSS treatment. b Representative image of tumor and adjacent nontumor tissues in the mouse colon on day 77 after AOM injection. Colon sections were stained with hematoxylin eosin (H E) ( n = 20 mice). Scale bar, 200 μm. c mRNA samples from tumor and nontumor tissues were analyzed using qPCR to determine the expression levels of the indicated genes. Results are mean ± SEM ( n = 6 mice). Results are representative of two independent experiments. d – f From colonic tumor tissues of Il11-Egfp reporter mice, single-cell suspensions were prepared, and percentages of IL-11 + (EGFP + ) cells were determined. Representative flow cytometry images are shown ( d ). Results are mean ± SEM ( n = 7 mice). Cells were stained with the indicated antibodies, and marker expression on EGFP + cells was analyzed by flow cytometry. A representative dot plot from three independent experiments shows the percentages of EGFP + cells expressing each marker ( n = 5 mice except for CD34 where n = 4 mice) ( e ). Percentages of EGFP + cells among podoplanin + cells ( f ). Results are mean ± SEM ( n = 5 mice). g Nontumor and tumor tissue sections were stained with anti-GFP antibody ( n = 4 mice). Scale bars, 100 μm. h – l Tumor sections were stained with anti-GFP along with anti-IL-11 ( h ) ( n = 4 mice), anti-E-cadherin ( j ) ( n = 4 mice), or anti-Ki67 ( k ) and anti-podoplanin ( k ) antibodies ( n = 5 mice). The right-hand panels show enlarged images of white boxes from the left-hand panels. White arrowheads indicate EGFP + cells expressing the respective markers shown in red. IL-11 + and EGFP + cell numbers were calculated, and IL-11 + /EGFP + areas as percentages of the total area are shown ( i ). Ki67 + and EGFP + cell numbers were calculated, and are shown as percentages of the total area ( l ). Results are mean ± SEM ( n = 5 mice). Scale bars, 100 μm. Statistical significance was determined using the two-tailed unpaired Student’s t -test ( c , d ). Source data are provided as a Source Data file.

    Techniques Used: Mouse Assay, Injection, Staining, Real-time Polymerase Chain Reaction, Expressing, Flow Cytometry, Marker, Two Tailed Test

    IL-11 + fibroblasts express genes associated with cell proliferation and tissue repair. Il11-Egfp mice were treated with DSS. On day 7 after DSS treatment, cells were isolated from colons of Il11-Egfp reporter mice, and IL-11 + cells (EGFP + ) and IL-11 − (EGFP − ) cells among Ter119 − CD45 − CD31 − EpCAM − cell populations were sorted by flow cytometry. We isolated mRNA from IL-11 − and from IL-11 + cells and analyzed both using RNA-seq ( n = 3 mice). a Verification of enrichment of IL-11 + cells by flow cytometry. Expression of Il11 and Egfp mRNAs was determined by qPCR. Results are mean ± SEM ( n = 5 mice). b Volcano plot of whole genes. The horizontal line indicates genes differentially regulated in IL-11 + cells compared with IL-11 − cells, shown in log 2 . The vertical line indicates p- values, shown in −log 10 . Significantly upregulated and downregulated genes are indicated by red and blue dots, respectively. Several upregulated genes are plotted. c Gene ontology (GO) terms that were significantly enriched in IL-11 + cells compared with IL-11 − cells. GO enrichment analysis of differentially expressed genes were performed using the DAVID Bioinformatics Resources. d Heat map of enriched genes in IL-11 + fibroblasts compared with IL-11 − fibroblasts. Color code for heatmap indicates Z-score of gene expression. e Expression of I111ra is not different between IL-11 + and IL-11 − fibroblasts. Expression of Il11ra mRNA was determined by qPCR. Results are mean ± SEM ( n = 5 mice). f Gene set enrichment analysis of IAFs-related genes in IL-11 + and IL-11 − fibroblasts. FDR false discovery rate, NES normalized enrichment score. Statistical significance was determined by using the two-tailed unpaired Student’s t -test ( a , e ) or two-tailed Kolmogorov-Smirnov test ( f ). The estimation of logFC and adjusted p -value were calculated using edgeR package in R ( b , c ).
    Figure Legend Snippet: IL-11 + fibroblasts express genes associated with cell proliferation and tissue repair. Il11-Egfp mice were treated with DSS. On day 7 after DSS treatment, cells were isolated from colons of Il11-Egfp reporter mice, and IL-11 + cells (EGFP + ) and IL-11 − (EGFP − ) cells among Ter119 − CD45 − CD31 − EpCAM − cell populations were sorted by flow cytometry. We isolated mRNA from IL-11 − and from IL-11 + cells and analyzed both using RNA-seq ( n = 3 mice). a Verification of enrichment of IL-11 + cells by flow cytometry. Expression of Il11 and Egfp mRNAs was determined by qPCR. Results are mean ± SEM ( n = 5 mice). b Volcano plot of whole genes. The horizontal line indicates genes differentially regulated in IL-11 + cells compared with IL-11 − cells, shown in log 2 . The vertical line indicates p- values, shown in −log 10 . Significantly upregulated and downregulated genes are indicated by red and blue dots, respectively. Several upregulated genes are plotted. c Gene ontology (GO) terms that were significantly enriched in IL-11 + cells compared with IL-11 − cells. GO enrichment analysis of differentially expressed genes were performed using the DAVID Bioinformatics Resources. d Heat map of enriched genes in IL-11 + fibroblasts compared with IL-11 − fibroblasts. Color code for heatmap indicates Z-score of gene expression. e Expression of I111ra is not different between IL-11 + and IL-11 − fibroblasts. Expression of Il11ra mRNA was determined by qPCR. Results are mean ± SEM ( n = 5 mice). f Gene set enrichment analysis of IAFs-related genes in IL-11 + and IL-11 − fibroblasts. FDR false discovery rate, NES normalized enrichment score. Statistical significance was determined by using the two-tailed unpaired Student’s t -test ( a , e ) or two-tailed Kolmogorov-Smirnov test ( f ). The estimation of logFC and adjusted p -value were calculated using edgeR package in R ( b , c ).

    Techniques Used: Mouse Assay, Isolation, Flow Cytometry, RNA Sequencing Assay, Expressing, Real-time Polymerase Chain Reaction, Two Tailed Test

    IL-11 + fibroblasts appear in the colon in DSS-treated mice and express stromal cell markers. a Kinetics of Il11 expression in the colon after DSS treatment. WT mice were treated with 1.5% DSS in drinking water for 5 days, followed by a change to regular water. Expression of Il11 in the colon of mice on the indicated days after DSS treatment was determined using qPCR. Results are mean ± SEM. n = 8 (day 0), 9 (day 4), 7 (day 7), or 11 (day 9) mice; pooled data from two independent experiments. b , c Appearance of IL-11 + cells in submucosal tissues of the colon in Il11-Egfp reporter mice on post-DSS treatment day 8 ( b ) or day 1 ( c ). Colon tissue sections from untreated or DSS-treated Il11-Egfp reporter mice were H E stained or immunostained with anti-GFP antibody. n = 10 (day 7~8) and 2 (day 1) mice. Right panels show enlargements of the boxes ( c ). Scale bar, 100 μm. d – f Characterization of cell surface markers on IL-11 + cells. WT and Il11-Egfp reporter mice were untreated or treated with DSS as in ( a ), and EGFP + (IL-11 + ) cells were analyzed by flow cytometry. Representative dot plots of untreated or DSS-treated Il11-Egfp reporter mice on day 7 ( d ). Percentages of IL-11 + cells from the colon before and on day 1 or day 7 after DSS treatment ( e ). Results are mean ± SEM. n = 5 (untreated WT on day 1), 4 (untreated Il11-Egfp on day 1), 7 (DSS-treated Il11-Egfp on day 1), 6 (untreated Il11-Egfp on day 7), or 4 (DSS-treated Il11-Egfp on day 7) mice. Cells were stained with the indicated antibodies, and marker expression was analyzed on EGFP + cells ( f ). Representative dot plot of four independent experiments ( n = 4 mice). g Representative immunostaining of IL-11 + cells. Colon tissue sections were prepared from Il11-Egfp reporter mice as in ( b ) and immunostained with the indicated antibodies and anti-GFP antibody ( n = 4 mice). Results are merged images. Right panels are enlarged images from the boxes. White arrowheads indicate merged cells. h , i IL-11 + cells do not proliferate in situ. Il11-Egfp reporter mice were treated with DSS as in ( a ) and intraperitoneally injected BrdU (40 mg/kg) on day 6. On day 7, colon sections were prepared and stained with anti-GFP and anti-BrdU antibodies ( n = 5 mice). Scale bars, 100 μm. BrdU + and EGFP + cells were counted, and the percentages of BrdU + cells among EGFP + cells were plotted ( i ). Results are mean ± SEM ( n = 5 mice). Statistical significance was determined using the one-way ANOVA with Tukey’s multiple comparison test ( a , left graph in e ) or the unpaired two-tailed Student’s t -test (right graph in e ). Source data are provided as a Source Data file.
    Figure Legend Snippet: IL-11 + fibroblasts appear in the colon in DSS-treated mice and express stromal cell markers. a Kinetics of Il11 expression in the colon after DSS treatment. WT mice were treated with 1.5% DSS in drinking water for 5 days, followed by a change to regular water. Expression of Il11 in the colon of mice on the indicated days after DSS treatment was determined using qPCR. Results are mean ± SEM. n = 8 (day 0), 9 (day 4), 7 (day 7), or 11 (day 9) mice; pooled data from two independent experiments. b , c Appearance of IL-11 + cells in submucosal tissues of the colon in Il11-Egfp reporter mice on post-DSS treatment day 8 ( b ) or day 1 ( c ). Colon tissue sections from untreated or DSS-treated Il11-Egfp reporter mice were H E stained or immunostained with anti-GFP antibody. n = 10 (day 7~8) and 2 (day 1) mice. Right panels show enlargements of the boxes ( c ). Scale bar, 100 μm. d – f Characterization of cell surface markers on IL-11 + cells. WT and Il11-Egfp reporter mice were untreated or treated with DSS as in ( a ), and EGFP + (IL-11 + ) cells were analyzed by flow cytometry. Representative dot plots of untreated or DSS-treated Il11-Egfp reporter mice on day 7 ( d ). Percentages of IL-11 + cells from the colon before and on day 1 or day 7 after DSS treatment ( e ). Results are mean ± SEM. n = 5 (untreated WT on day 1), 4 (untreated Il11-Egfp on day 1), 7 (DSS-treated Il11-Egfp on day 1), 6 (untreated Il11-Egfp on day 7), or 4 (DSS-treated Il11-Egfp on day 7) mice. Cells were stained with the indicated antibodies, and marker expression was analyzed on EGFP + cells ( f ). Representative dot plot of four independent experiments ( n = 4 mice). g Representative immunostaining of IL-11 + cells. Colon tissue sections were prepared from Il11-Egfp reporter mice as in ( b ) and immunostained with the indicated antibodies and anti-GFP antibody ( n = 4 mice). Results are merged images. Right panels are enlarged images from the boxes. White arrowheads indicate merged cells. h , i IL-11 + cells do not proliferate in situ. Il11-Egfp reporter mice were treated with DSS as in ( a ) and intraperitoneally injected BrdU (40 mg/kg) on day 6. On day 7, colon sections were prepared and stained with anti-GFP and anti-BrdU antibodies ( n = 5 mice). Scale bars, 100 μm. BrdU + and EGFP + cells were counted, and the percentages of BrdU + cells among EGFP + cells were plotted ( i ). Results are mean ± SEM ( n = 5 mice). Statistical significance was determined using the one-way ANOVA with Tukey’s multiple comparison test ( a , left graph in e ) or the unpaired two-tailed Student’s t -test (right graph in e ). Source data are provided as a Source Data file.

    Techniques Used: Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Staining, Flow Cytometry, Marker, Immunostaining, In Situ, Injection, Two Tailed Test

    12) Product Images from "Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice"

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    Journal: World Journal of Gastroenterology

    doi: 10.3748/wjg.v24.i16.1779

    Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P
    Figure Legend Snippet: Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P

    Techniques Used: Mouse Assay, Activity Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

    NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry, Cell Culture, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry

    CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P
    Figure Legend Snippet: CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry, Isolation, Cell Culture, Enzyme-linked Immunosorbent Assay

    iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.
    Figure Legend Snippet: iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.

    Techniques Used: Mouse Assay, Injection, Staining, Confocal Microscopy, Fluorescence

    Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P
    Figure Legend Snippet: Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P

    Techniques Used: Mouse Assay, Staining

    13) Product Images from "Fermented Pueraria Lobata extract ameliorates dextran sulfate sodium-induced colitis by reducing pro-inflammatory cytokines and recovering intestinal barrier function"

    Article Title: Fermented Pueraria Lobata extract ameliorates dextran sulfate sodium-induced colitis by reducing pro-inflammatory cytokines and recovering intestinal barrier function

    Journal: Laboratory Animal Research

    doi: 10.5625/lar.2016.32.3.151

    Effect of fPue on DSS-induced colitis in mice. A. Schedule for administration of 5% DSS and fPue. B. Assessment of disease activity index (DAI) by fecal analysis. C. Histological evaluation of DSS-induced colitis according to degree of epithelial cell loss, crypt damage, and infiltration of inflammatory cells. D. Histological figures of colon stained by H E. (a, mucosa; b, submucosa; c, muscularis; d, crypt) E. Histological figures to observe goblet cell loss by Alcian Blue staining. Numerical data were expressed as mean±standard deviation (n=7, * P
    Figure Legend Snippet: Effect of fPue on DSS-induced colitis in mice. A. Schedule for administration of 5% DSS and fPue. B. Assessment of disease activity index (DAI) by fecal analysis. C. Histological evaluation of DSS-induced colitis according to degree of epithelial cell loss, crypt damage, and infiltration of inflammatory cells. D. Histological figures of colon stained by H E. (a, mucosa; b, submucosa; c, muscularis; d, crypt) E. Histological figures to observe goblet cell loss by Alcian Blue staining. Numerical data were expressed as mean±standard deviation (n=7, * P

    Techniques Used: Mouse Assay, Activity Assay, Staining, Standard Deviation

    Evaluating a direct effect of fPue on recovery of tight junction proteins, using Caco-2 cells. A. Western blot analysis for expression of tight junction proteins, ZO-1 and Occludin after treatment of fPue with 2% DSS. B. Immunofluorescence assay for ZO-1 and Occludin on Caco-2 cells. DSS, dextran sulfate sodium; fPue, fermented form of Pueraria Lobata aqueous extract.
    Figure Legend Snippet: Evaluating a direct effect of fPue on recovery of tight junction proteins, using Caco-2 cells. A. Western blot analysis for expression of tight junction proteins, ZO-1 and Occludin after treatment of fPue with 2% DSS. B. Immunofluorescence assay for ZO-1 and Occludin on Caco-2 cells. DSS, dextran sulfate sodium; fPue, fermented form of Pueraria Lobata aqueous extract.

    Techniques Used: Western Blot, Expressing, Immunofluorescence

    14) Product Images from "Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis"

    Article Title: Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

    Journal: Cell Reports

    doi: 10.1016/j.celrep.2018.12.072

    Deletion of TLR4 in IMCs Reduces Tumorigenesis in the Apc min/+ Model of Sporadic Intestinal Cancer . One representative of three independent experiments performed in triplicates is presented. . Log2 fold-change of genes is shown. Red denotes high expression values, and blue denotes low expression values. (C and D) Total number (C) and size (D) of tumors per mouse in 4-month-old Apc min/+ Il1r1 IMCko mice (n = 14) and their littermate controls (n = 24). (E and F) Total number of tumors per mouse (E) and number of tumors per intestinal part (F) in 4-month-old Apc min/+ Tlr4 IMCko mice (n = 13) and their littermate controls (n = 20). The insert shows the number of tumors in the colon. (G and H) Mean tumor size (G) and distribution of tumors (H) per size in the two genotypes. (I) Representative BrdU and pSTAT3 staining in small intestinal tumors of Apc min/+ Tlr4 IMCko mice and their littermate controls. Scale bar = 50 μm. (J) Quantification of the number of BrdU + cells per tumor (n = 6 mice per genotype). (K) Mean signal intensity (MSI) of pSTAT3 (n = 12–14 tumors from 4 mice per genotype). (L) Gene expression analysis in tumors from Apc min/+ Tlr4 F/F and Apc min/+ Tlr4 IMCko mice (n = 6). Hprt was used for normalization. (M) Number of tumors per mouse in Tlr4 IMCko mice (n = 8) and their littermate controls (n = 8) at the end of the AOM/DSS protocol (one representative experiment of three performed). Data represent mean ± SEM. ∗ p
    Figure Legend Snippet: Deletion of TLR4 in IMCs Reduces Tumorigenesis in the Apc min/+ Model of Sporadic Intestinal Cancer . One representative of three independent experiments performed in triplicates is presented. . Log2 fold-change of genes is shown. Red denotes high expression values, and blue denotes low expression values. (C and D) Total number (C) and size (D) of tumors per mouse in 4-month-old Apc min/+ Il1r1 IMCko mice (n = 14) and their littermate controls (n = 24). (E and F) Total number of tumors per mouse (E) and number of tumors per intestinal part (F) in 4-month-old Apc min/+ Tlr4 IMCko mice (n = 13) and their littermate controls (n = 20). The insert shows the number of tumors in the colon. (G and H) Mean tumor size (G) and distribution of tumors (H) per size in the two genotypes. (I) Representative BrdU and pSTAT3 staining in small intestinal tumors of Apc min/+ Tlr4 IMCko mice and their littermate controls. Scale bar = 50 μm. (J) Quantification of the number of BrdU + cells per tumor (n = 6 mice per genotype). (K) Mean signal intensity (MSI) of pSTAT3 (n = 12–14 tumors from 4 mice per genotype). (L) Gene expression analysis in tumors from Apc min/+ Tlr4 F/F and Apc min/+ Tlr4 IMCko mice (n = 6). Hprt was used for normalization. (M) Number of tumors per mouse in Tlr4 IMCko mice (n = 8) and their littermate controls (n = 8) at the end of the AOM/DSS protocol (one representative experiment of three performed). Data represent mean ± SEM. ∗ p

    Techniques Used: Expressing, Mouse Assay, Staining

    Deletion of MyD88 in Intestinal Mesenchymal Cells Reduces Tumorigenesis in the Apc min/+ Model of Sporadic Intestinal Cancer (A and B) Total number of tumors per mouse (A) and number of tumors per intestinal part (B) in 4-month-old Apc min/+ Myd88 IMCko mice (n = 15) and their littermate controls (n = 18). The insert shows the number of colonic tumors. (C and D) Size of small intestinal tumors presented as mean tumor size (C) and distribution of tumors per size (D) in the two genotypes. (E) Representative BrdU and Tunel staining in small intestinal tumors of Apc min/+ Myd88 IMCko mice and their littermate controls. DAPI was used to stain the nuclei in the Tunel stainings. (F and G) Quantification of the number of BrdU + cells per tumor (F) and Tunel + cells (G) per field in equal-sized tumors (n = 6 mice per genotype). (H) Number of dysplastic lesions per mouse in 6-week-old Apc min/+ Myd88 IMCko and their littermate controls (n = 6–7 mice per genotype). (I) Number of tumors per mouse in Myd88 IMCko mice (n = 8) and their littermate controls (n = 7) at the end of the AOM/DSS protocol (one representative experiment of four performed). Data represent mean ± SEM. ∗∗ p
    Figure Legend Snippet: Deletion of MyD88 in Intestinal Mesenchymal Cells Reduces Tumorigenesis in the Apc min/+ Model of Sporadic Intestinal Cancer (A and B) Total number of tumors per mouse (A) and number of tumors per intestinal part (B) in 4-month-old Apc min/+ Myd88 IMCko mice (n = 15) and their littermate controls (n = 18). The insert shows the number of colonic tumors. (C and D) Size of small intestinal tumors presented as mean tumor size (C) and distribution of tumors per size (D) in the two genotypes. (E) Representative BrdU and Tunel staining in small intestinal tumors of Apc min/+ Myd88 IMCko mice and their littermate controls. DAPI was used to stain the nuclei in the Tunel stainings. (F and G) Quantification of the number of BrdU + cells per tumor (F) and Tunel + cells (G) per field in equal-sized tumors (n = 6 mice per genotype). (H) Number of dysplastic lesions per mouse in 6-week-old Apc min/+ Myd88 IMCko and their littermate controls (n = 6–7 mice per genotype). (I) Number of tumors per mouse in Myd88 IMCko mice (n = 8) and their littermate controls (n = 7) at the end of the AOM/DSS protocol (one representative experiment of four performed). Data represent mean ± SEM. ∗∗ p

    Techniques Used: Mouse Assay, TUNEL Assay, Staining

    15) Product Images from "Effects of Selenium on Colon Carcinogenesis Induced by Azoxymethane and Dextran Sodium Sulfate in Mouse Model with High-Iron Diet"

    Article Title: Effects of Selenium on Colon Carcinogenesis Induced by Azoxymethane and Dextran Sodium Sulfate in Mouse Model with High-Iron Diet

    Journal: Laboratory Animal Research

    doi: 10.5625/lar.2011.27.1.9

    Effect of Se on hepatic GPx-1 by western blot in mice fed the high Fe diet with different Se levels. The expression of GPx-1 was up-regulated in the high-Se group compared with the low-Se group. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abc Means not sharing common superscript letters are significantly different at P
    Figure Legend Snippet: Effect of Se on hepatic GPx-1 by western blot in mice fed the high Fe diet with different Se levels. The expression of GPx-1 was up-regulated in the high-Se group compared with the low-Se group. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abc Means not sharing common superscript letters are significantly different at P

    Techniques Used: Western Blot, Mouse Assay, Expressing

    TUNEL assay for apoptotic nuclei in distal colon sections of mice fed high-Fe diet with different Se levels. The TUNEL-positive cells were increased by dietary Se in a dose-dependent manner. Vehicle (A), AOM/DSS+NFe+MSe (positive control, B), AOM/DSS+HFe+LSe (C), AOM/DSS+HFe+MSe (D), AOM/DSS+HFe+HSe (E).
    Figure Legend Snippet: TUNEL assay for apoptotic nuclei in distal colon sections of mice fed high-Fe diet with different Se levels. The TUNEL-positive cells were increased by dietary Se in a dose-dependent manner. Vehicle (A), AOM/DSS+NFe+MSe (positive control, B), AOM/DSS+HFe+LSe (C), AOM/DSS+HFe+MSe (D), AOM/DSS+HFe+HSe (E).

    Techniques Used: TUNEL Assay, Mouse Assay, Positive Control

    Immunohistochemistry of PCNA in the colon of mice fed the low Fe diet with different Se levels. The PCNA-positive cells were increased by treatment with AOM/DSS, but they were reduced by co-administration of a high concentration of Se. Vehicle (A), AOM/DSS+NFe+MSe (positive control, B), AOM/DSS+HFe+LSe (C), AOM/DSS+HFe+MSe (D), AOM/DSS+HFe+HSe (E).
    Figure Legend Snippet: Immunohistochemistry of PCNA in the colon of mice fed the low Fe diet with different Se levels. The PCNA-positive cells were increased by treatment with AOM/DSS, but they were reduced by co-administration of a high concentration of Se. Vehicle (A), AOM/DSS+NFe+MSe (positive control, B), AOM/DSS+HFe+LSe (C), AOM/DSS+HFe+MSe (D), AOM/DSS+HFe+HSe (E).

    Techniques Used: Immunohistochemistry, Mouse Assay, Concentration Assay, Positive Control

    Hepatic Fe levels in mice fed the high Fe diet. Fe concentration was determined using an inductively coupled plasma spectrophotometer. High Fe diet significantly increased hepatic Fe levels compared with the control group. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abc Means not sharing common superscript letters are significantly different at P
    Figure Legend Snippet: Hepatic Fe levels in mice fed the high Fe diet. Fe concentration was determined using an inductively coupled plasma spectrophotometer. High Fe diet significantly increased hepatic Fe levels compared with the control group. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abc Means not sharing common superscript letters are significantly different at P

    Techniques Used: Mouse Assay, Concentration Assay, Spectrophotometry

    Hepatic Se levels in mice fed the high Fe diet with different Se levels. The Se concentration was determined using an inductively coupled plasma mass spectrophotometer. The hepatic Se levels were dependent on dietary Se levels. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. ab Means not sharing common superscript letters are significantly different at P
    Figure Legend Snippet: Hepatic Se levels in mice fed the high Fe diet with different Se levels. The Se concentration was determined using an inductively coupled plasma mass spectrophotometer. The hepatic Se levels were dependent on dietary Se levels. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. ab Means not sharing common superscript letters are significantly different at P

    Techniques Used: Mouse Assay, Concentration Assay, Spectrophotometry

    Effect of Se on hepatic MDA levels in mice fed the high Fe diet with different Se levels. The MDA levels were decreased by dietary Se in a dose-dependent manner. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abcd Means not sharing common superscript letters are significantly different at P
    Figure Legend Snippet: Effect of Se on hepatic MDA levels in mice fed the high Fe diet with different Se levels. The MDA levels were decreased by dietary Se in a dose-dependent manner. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. abcd Means not sharing common superscript letters are significantly different at P

    Techniques Used: Multiple Displacement Amplification, Mouse Assay

    Change in the body weights of mice fed the high Fe diet. All AOM/DSS-treated groups showed a low body weight compared with the vehicle group during experimental periods. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. ab Means not sharing common superscript letters are significantly different at P
    Figure Legend Snippet: Change in the body weights of mice fed the high Fe diet. All AOM/DSS-treated groups showed a low body weight compared with the vehicle group during experimental periods. AOM: azoxymethane, DSS: dextran sodium sulfate, HFe: high-Fe diet (450 ppm), LSe: low-Se diet (0.02 ppm), MSe: medium-Se diet (0.1 ppm), HSe: high-Se diet (0.5 ppm). Data were represented as mean±SE. ab Means not sharing common superscript letters are significantly different at P

    Techniques Used: Mouse Assay

    16) Product Images from "Neural innervation stimulates splenic TFF2 to arrest myeloid cell expansion and cancer"

    Article Title: Neural innervation stimulates splenic TFF2 to arrest myeloid cell expansion and cancer

    Journal: Nature Communications

    doi: 10.1038/ncomms10517

    TFF2 status was associated with the expansion of IMC/MDSCs and development of colorectal cancer. ( a , b ) DSS treatment results in splenomegaly ( a ) and accumulation of CD11b + Gr-1 + cells ( b ) in Tff2-null and wild-type mice, but not in CD2–Tff2 counterparts. Representative data from two independent experiments, 3–6 mice per group for each time point. NS, non-significant, * P
    Figure Legend Snippet: TFF2 status was associated with the expansion of IMC/MDSCs and development of colorectal cancer. ( a , b ) DSS treatment results in splenomegaly ( a ) and accumulation of CD11b + Gr-1 + cells ( b ) in Tff2-null and wild-type mice, but not in CD2–Tff2 counterparts. Representative data from two independent experiments, 3–6 mice per group for each time point. NS, non-significant, * P

    Techniques Used: Mouse Assay

    TFF2 is expressed in CD4 + memory T cells and regulated by the vagus nerve. ( a ) Identification of TFF2 peptide in normal spleen of wild-type mice by western blot. ( b , c ) Time-course change of the TFF2 protein ( b ) and mRNA ( c ) in spleen of wild-type mice after 2.5% DSS treatment. Data shown are representative of two experiments for each analysis. Data is mean±s.e.m of triplicate determinations, ** P
    Figure Legend Snippet: TFF2 is expressed in CD4 + memory T cells and regulated by the vagus nerve. ( a ) Identification of TFF2 peptide in normal spleen of wild-type mice by western blot. ( b , c ) Time-course change of the TFF2 protein ( b ) and mRNA ( c ) in spleen of wild-type mice after 2.5% DSS treatment. Data shown are representative of two experiments for each analysis. Data is mean±s.e.m of triplicate determinations, ** P

    Techniques Used: Mouse Assay, Western Blot

    TFF2 inhibited cancer through suppression of MDSC proliferation. ( a , b ) Expansion of Gr-1 + cells in red pulp due to their high proliferation in Tff2-null mice treated with DSS. Ki67 (brown) and Gr-1 (red) immunostaining of spleens from DSS-challenged mice. Scale bar, 500 μm ( a ) and 100 μm ( b ). ( c ) Recombinant TFF2 suppresses proliferation of IMCs in response to TFF2 in vitro. Sorted CD11b + Gr-1 + cells from spleen of DSS-treated Tff2-null mice were GM-CSF with or without TFF2 at indicated concentrations. Proliferation was measured by BrdU uptake. Values are mean±s.e.m. of 3–4 replicates (* P
    Figure Legend Snippet: TFF2 inhibited cancer through suppression of MDSC proliferation. ( a , b ) Expansion of Gr-1 + cells in red pulp due to their high proliferation in Tff2-null mice treated with DSS. Ki67 (brown) and Gr-1 (red) immunostaining of spleens from DSS-challenged mice. Scale bar, 500 μm ( a ) and 100 μm ( b ). ( c ) Recombinant TFF2 suppresses proliferation of IMCs in response to TFF2 in vitro. Sorted CD11b + Gr-1 + cells from spleen of DSS-treated Tff2-null mice were GM-CSF with or without TFF2 at indicated concentrations. Proliferation was measured by BrdU uptake. Values are mean±s.e.m. of 3–4 replicates (* P

    Techniques Used: Mouse Assay, Immunostaining, Recombinant, In Vitro

    Adenoviral delivery of TFF2 reduced colorectal carcinogenesis. ( a ) Detection of recombinant TFF2 by western blot in serum from Tff2-null , NOD-SCID and WT mice 5 days after Ad-m Tff2 treatment (5 × 10 8 pfu per mouse). ( b , c ) Ad- Tff2 reduced splenic CD11b + Gr-1 + cells compared to the Ad-Fc treated controls in both Tff2-null ( b ) and wild-type mice ( c ) following AOM/DSS protocol, ** P
    Figure Legend Snippet: Adenoviral delivery of TFF2 reduced colorectal carcinogenesis. ( a ) Detection of recombinant TFF2 by western blot in serum from Tff2-null , NOD-SCID and WT mice 5 days after Ad-m Tff2 treatment (5 × 10 8 pfu per mouse). ( b , c ) Ad- Tff2 reduced splenic CD11b + Gr-1 + cells compared to the Ad-Fc treated controls in both Tff2-null ( b ) and wild-type mice ( c ) following AOM/DSS protocol, ** P

    Techniques Used: Recombinant, Western Blot, Mouse Assay

    17) Product Images from "Targeted metabolomics identifies the cytochrome P450 monooxygenase eicosanoid pathway as a novel therapeutic target of colon tumorigenesis"

    Article Title: Targeted metabolomics identifies the cytochrome P450 monooxygenase eicosanoid pathway as a novel therapeutic target of colon tumorigenesis

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-18-3221

    Compared with Cyp2c +/+ mice, the AOM/DSS-induced colon tumorigenesis is reduced in Cyp2c +/− mice. (A) Scheme of animal experiment. (B) Quantification of colon tumorigenesis (n = 12 per group). (C) H E histology, and immunohistochemical staining of PCNA and β-catenin in colon (n = 7 per group, scale bar: 50 μm). (D) Expression of pro-inflammatory and pro-tumorigenic genes, and Cyp monooxygenase (using Cyp2c38 as a marker) in colon (n = 10-12 per group). (E) Concentrations of CYP monooxygenase-produced metabolites in colon (n = 12 per group). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.
    Figure Legend Snippet: Compared with Cyp2c +/+ mice, the AOM/DSS-induced colon tumorigenesis is reduced in Cyp2c +/− mice. (A) Scheme of animal experiment. (B) Quantification of colon tumorigenesis (n = 12 per group). (C) H E histology, and immunohistochemical staining of PCNA and β-catenin in colon (n = 7 per group, scale bar: 50 μm). (D) Expression of pro-inflammatory and pro-tumorigenic genes, and Cyp monooxygenase (using Cyp2c38 as a marker) in colon (n = 10-12 per group). (E) Concentrations of CYP monooxygenase-produced metabolites in colon (n = 12 per group). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.

    Techniques Used: Mouse Assay, Immunohistochemistry, Staining, Expressing, Marker, Produced

    CYP monooxygenase-produced eicosanoid metabolites are increased in the plasma and colon of AOM/DSS-induced colon cancer mice. (A) Scheme of animal experiment. (B) Quantification of colon tumor in mice (n = 6 in control group, and n = 10 in colon cancer group). (C) Gene expression of Tnf-α, Mcp-1, Il-6 and Cox-2 in colon (n = 4 per group). (D-G) Concentrations of CYP monooxygenase-produced EpFAs in plasma and colon (n = 6-10 per group). (H) Expression of Pla2 , Cyp monooxygenases , and Ephx2 (encoding sEH) in colon (n = 4-6 per group). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.
    Figure Legend Snippet: CYP monooxygenase-produced eicosanoid metabolites are increased in the plasma and colon of AOM/DSS-induced colon cancer mice. (A) Scheme of animal experiment. (B) Quantification of colon tumor in mice (n = 6 in control group, and n = 10 in colon cancer group). (C) Gene expression of Tnf-α, Mcp-1, Il-6 and Cox-2 in colon (n = 4 per group). (D-G) Concentrations of CYP monooxygenase-produced EpFAs in plasma and colon (n = 6-10 per group). (H) Expression of Pla2 , Cyp monooxygenases , and Ephx2 (encoding sEH) in colon (n = 4-6 per group). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.

    Techniques Used: Produced, Mouse Assay, Expressing

    EpOME exaggerates AOM/DSS-induced colon tumorigenesis in vivo . (A) Scheme of animal experiment to test the effect of 12,13-EpOME (dose = 2 mg/kg/day, administered via mini-pump) on colon tumorigenesis. (B) Quantification of colon tumorigenesis in mice (n = 8-9 per group). (C) Expression of pro-inflammatory and pro-tumorigenic genes in colon (n = 6-8 per group). (D) Quantification of CD45 + and CD45 + F4/80 + immune cells in colon (n = 7-8 per group). (E) H E histology, and immunohistochemical staining of PCNA and β-catenin in colon (n = 6-7 per group, scale bar: 50 μm). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.
    Figure Legend Snippet: EpOME exaggerates AOM/DSS-induced colon tumorigenesis in vivo . (A) Scheme of animal experiment to test the effect of 12,13-EpOME (dose = 2 mg/kg/day, administered via mini-pump) on colon tumorigenesis. (B) Quantification of colon tumorigenesis in mice (n = 8-9 per group). (C) Expression of pro-inflammatory and pro-tumorigenic genes in colon (n = 6-8 per group). (D) Quantification of CD45 + and CD45 + F4/80 + immune cells in colon (n = 7-8 per group). (E) H E histology, and immunohistochemical staining of PCNA and β-catenin in colon (n = 6-7 per group, scale bar: 50 μm). The results are expressed as mean ± SEM. The statistical significance of two groups was determined using Student’s t test or Wilcoxon-Mann test.

    Techniques Used: In Vivo, Mouse Assay, Expressing, Immunohistochemistry, Staining

    18) Product Images from "G protein-coupled receptor GPR55 promotes colorectal cancer and has opposing effects to cannabinoid receptor 1"

    Article Title: G protein-coupled receptor GPR55 promotes colorectal cancer and has opposing effects to cannabinoid receptor 1

    Journal: International journal of cancer

    doi: 10.1002/ijc.31030

    GPR55 promotes colorectal cancer. ( A ) In a model of colitis-associated CRC, GPR55 -/- mice (n=36) had less tumors and smaller total tumor areas than their wild-type littermates (WT, n=44). ( B ) H E staining from sections of tumors in the colon induced by AOM+DSS in GPR55 -/- (left panel) and wild-type mice (right panel). Images are representative of 4 mice of each cohort. Inserts in the right upper corner of the images show adenomas in GPR55 -/- and wild-type mice in lower magnification (size bars: 500 µm). ( C ) Pharmacological inhibition of GPR55 with CID16020046 (5 mg/kg) reduced tumor numbers and areas compared to vehicle treatment (n=9 for both groups). ( D ) Tumor numbers and areas were reduced in GPR55 -/- mice (n=27) compared to wild-type mice (n=18) in a model of spontaneous tumor progression. ( E ) In CRC patients, high GPR55 mRNA expression in tumor tissue was significantly associated with reduced relapse-free survival ( P =.016, log-rank test). ( F ) Cellular detection of GPR55 mRNA with RNAscope ® 2.5 Chromogenic Assay using 3,3'-diaminobenzidine (DAB) as a chromogene (brown color). Sections were counterstained with hematoxylin (blue). Sections of colonic mucosa of healthy wild-type (WT) mice showed GPR55 expression (left panel), while the staining was absent in knockout (GPR55 -/- ) controls (middle panel). Tumors of wild-type mice expressed GPR55 mRNA in various cells (right panel). Arrows point at DAB precipitates at the sites of GPR55 mRNA expression in cells. Arrowheads denote heterochromatin (blue) in cell nuclei. Symbols depict data from individual mice, and bars show the mean. ** P
    Figure Legend Snippet: GPR55 promotes colorectal cancer. ( A ) In a model of colitis-associated CRC, GPR55 -/- mice (n=36) had less tumors and smaller total tumor areas than their wild-type littermates (WT, n=44). ( B ) H E staining from sections of tumors in the colon induced by AOM+DSS in GPR55 -/- (left panel) and wild-type mice (right panel). Images are representative of 4 mice of each cohort. Inserts in the right upper corner of the images show adenomas in GPR55 -/- and wild-type mice in lower magnification (size bars: 500 µm). ( C ) Pharmacological inhibition of GPR55 with CID16020046 (5 mg/kg) reduced tumor numbers and areas compared to vehicle treatment (n=9 for both groups). ( D ) Tumor numbers and areas were reduced in GPR55 -/- mice (n=27) compared to wild-type mice (n=18) in a model of spontaneous tumor progression. ( E ) In CRC patients, high GPR55 mRNA expression in tumor tissue was significantly associated with reduced relapse-free survival ( P =.016, log-rank test). ( F ) Cellular detection of GPR55 mRNA with RNAscope ® 2.5 Chromogenic Assay using 3,3'-diaminobenzidine (DAB) as a chromogene (brown color). Sections were counterstained with hematoxylin (blue). Sections of colonic mucosa of healthy wild-type (WT) mice showed GPR55 expression (left panel), while the staining was absent in knockout (GPR55 -/- ) controls (middle panel). Tumors of wild-type mice expressed GPR55 mRNA in various cells (right panel). Arrows point at DAB precipitates at the sites of GPR55 mRNA expression in cells. Arrowheads denote heterochromatin (blue) in cell nuclei. Symbols depict data from individual mice, and bars show the mean. ** P

    Techniques Used: Mouse Assay, Staining, Inhibition, Expressing, Chromogenic Assay, Knock-Out

    19) Product Images from "Activation of Aryl Hydrocarbon Receptor (AhR) Leads to Reciprocal Epigenetic Regulation of FoxP3 and IL-17 Expression and Amelioration of Experimental Colitis"

    Article Title: Activation of Aryl Hydrocarbon Receptor (AhR) Leads to Reciprocal Epigenetic Regulation of FoxP3 and IL-17 Expression and Amelioration of Experimental Colitis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0023522

    Change in body weight, histological characterization, and severity of colitis in mice after DSS induction and TCDD treatment. A. We used 4 groups of C57BL/6 mice: those that received VEH alone, TCDD (25 µg/kg body weight) alone, DSS+VEH, or a combination of DSS+TCDD. In DSS mice, TCDD was given as a single dose on the first day of DSS exposure. After seven days, DSS was replaced with a water cycle ( ad libitum ) for another seven days. The body weight of the mice was recorded daily. The statistical significance difference between each groups were assessed by using Mann-Whitney U Test. Data represents the mean of three experiment involving 6 mice per group. There was statistically significant difference between DSS+VEH vs DSS+TCDD groups (p
    Figure Legend Snippet: Change in body weight, histological characterization, and severity of colitis in mice after DSS induction and TCDD treatment. A. We used 4 groups of C57BL/6 mice: those that received VEH alone, TCDD (25 µg/kg body weight) alone, DSS+VEH, or a combination of DSS+TCDD. In DSS mice, TCDD was given as a single dose on the first day of DSS exposure. After seven days, DSS was replaced with a water cycle ( ad libitum ) for another seven days. The body weight of the mice was recorded daily. The statistical significance difference between each groups were assessed by using Mann-Whitney U Test. Data represents the mean of three experiment involving 6 mice per group. There was statistically significant difference between DSS+VEH vs DSS+TCDD groups (p

    Techniques Used: Mouse Assay, MANN-WHITNEY

    20) Product Images from "S1PR4 ablation reduces tumor growth and improves chemotherapy via CD8+ T cell expansion"

    Article Title: S1PR4 ablation reduces tumor growth and improves chemotherapy via CD8+ T cell expansion

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI136928

    S1PR4 ablation promotes CD8 + T cell expansion in a cell-intrinsic manner. ( A ) Venn diagram and the gene list show shared and divergent up- or downregulated genes in PyMT tumor-derived CD8 + T cells and total AOM/DSS-treated colons (day 84) comparing WT and S1PR4-KO mice. Genes selected for in vitro validation are highlighted in green. ( B and C ) Absolute number of WT and S1PR4-KO CD8 + T cells either untreated (w/o) or treated with ( B ) 0.5 μM PI3K inhibitor (Ly294002) or ( C ) 5 μM LTA4H inhibitor (SC 57461A) at day 2. One representative experiment with 5 independent biological replicates is shown, which was repeated 3 times with similar outcomes. ( D – I ) PyMT tumor spheroids were cocultured with WT and S1PR4-KO CD8 + T cells. One representative experiment with 5 independent biological replicates (each containing means of 6 technical replicates) is shown. ( D – F ) PyMT spheroid size upon coculture with untreated (black), Ly294002-treated (green), or SC 57461A–treated (red) CD8 + T cells over 6 days ( D and E ) and at day 6 ( F ) after initial activation with representative photographs ( G – I ). Scale bars: 200 μm. ( J ) Intracellular staining of p-AKT in NTC or PIK3AP1 siRNA-treated WT and S1PR4-KO CD8 + T cells 30 minutes after activation ( n = 4). p-AKT expression is shown as MFI. ( K ) LTB4 concentration in supernatants of WT and S1PR4-KO CD8 + T cells 1 day after activation determined by ELISA ( n = 5). ( L and M ) Absolute number of S1PR4 agonist (Cym 50308) or antagonist (Cym 50358) pretreated CD8 + T cells either untreated (w/o) or treated with 20 μM PGP 6 days ( L ) or 8 days ( M ) after activation ( n = 5). Means ± SEM; 1-way ANOVA ( B – F and J ) or 2-way ANOVA ( L and M ), each with Holm-Šidák correction; * P
    Figure Legend Snippet: S1PR4 ablation promotes CD8 + T cell expansion in a cell-intrinsic manner. ( A ) Venn diagram and the gene list show shared and divergent up- or downregulated genes in PyMT tumor-derived CD8 + T cells and total AOM/DSS-treated colons (day 84) comparing WT and S1PR4-KO mice. Genes selected for in vitro validation are highlighted in green. ( B and C ) Absolute number of WT and S1PR4-KO CD8 + T cells either untreated (w/o) or treated with ( B ) 0.5 μM PI3K inhibitor (Ly294002) or ( C ) 5 μM LTA4H inhibitor (SC 57461A) at day 2. One representative experiment with 5 independent biological replicates is shown, which was repeated 3 times with similar outcomes. ( D – I ) PyMT tumor spheroids were cocultured with WT and S1PR4-KO CD8 + T cells. One representative experiment with 5 independent biological replicates (each containing means of 6 technical replicates) is shown. ( D – F ) PyMT spheroid size upon coculture with untreated (black), Ly294002-treated (green), or SC 57461A–treated (red) CD8 + T cells over 6 days ( D and E ) and at day 6 ( F ) after initial activation with representative photographs ( G – I ). Scale bars: 200 μm. ( J ) Intracellular staining of p-AKT in NTC or PIK3AP1 siRNA-treated WT and S1PR4-KO CD8 + T cells 30 minutes after activation ( n = 4). p-AKT expression is shown as MFI. ( K ) LTB4 concentration in supernatants of WT and S1PR4-KO CD8 + T cells 1 day after activation determined by ELISA ( n = 5). ( L and M ) Absolute number of S1PR4 agonist (Cym 50308) or antagonist (Cym 50358) pretreated CD8 + T cells either untreated (w/o) or treated with 20 μM PGP 6 days ( L ) or 8 days ( M ) after activation ( n = 5). Means ± SEM; 1-way ANOVA ( B – F and J ) or 2-way ANOVA ( L and M ), each with Holm-Šidák correction; * P

    Techniques Used: Derivative Assay, Mouse Assay, In Vitro, Activation Assay, Staining, Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay

    S1PR4 signaling does not affect initial inflammation in the AOM/DSS model of colitis-associated cancer. ( A ) Experimental outline of the AOM/DSS model applied to WT and S1PR4-KO mice. ( B ) Weight of AOM/DSS-treated WT and S1PR4-KO mice as a percentage of weight at the initiation of treatment ( n = 9). ( C and D ) Relative amounts of CD45 + leukocytes ( C ) and immune cell populations ( D ) in the LP of WT and S1PR4-KO mice at day 0 ( n = 6), day 8 ( n = 8), day 15 ( n = 4), and day 84 ( n = 9) analyzed by flow cytometry. ( E ) Representative pictures of WT and S1PR4-KO AOM/DSS-treated colon tissue at day 8 stained with H E. Scale bars: 1 mm; scale bars of magnified areas:100 μm. ( F ) Colon weight-to-length ratio determined for WT and KO AOM/DSS-treated mice at days 0 (WT: n = 7, KO: n = 8), 8 ( n = 4), 15 ( n = 5), and 84 ( n = 10). Means ± SEM; 2-tailed Student’s t test; * P
    Figure Legend Snippet: S1PR4 signaling does not affect initial inflammation in the AOM/DSS model of colitis-associated cancer. ( A ) Experimental outline of the AOM/DSS model applied to WT and S1PR4-KO mice. ( B ) Weight of AOM/DSS-treated WT and S1PR4-KO mice as a percentage of weight at the initiation of treatment ( n = 9). ( C and D ) Relative amounts of CD45 + leukocytes ( C ) and immune cell populations ( D ) in the LP of WT and S1PR4-KO mice at day 0 ( n = 6), day 8 ( n = 8), day 15 ( n = 4), and day 84 ( n = 9) analyzed by flow cytometry. ( E ) Representative pictures of WT and S1PR4-KO AOM/DSS-treated colon tissue at day 8 stained with H E. Scale bars: 1 mm; scale bars of magnified areas:100 μm. ( F ) Colon weight-to-length ratio determined for WT and KO AOM/DSS-treated mice at days 0 (WT: n = 7, KO: n = 8), 8 ( n = 4), 15 ( n = 5), and 84 ( n = 10). Means ± SEM; 2-tailed Student’s t test; * P

    Techniques Used: Mouse Assay, Flow Cytometry, Staining

    S1PR4 ablation restricts tumor formation of colitis-associated cancer and induces epithelial CD8 + T cell expansion. ( A ) Representative images of WT and S1PR4-KO AOM/DSS-treated colons at day 84 stained with H E. Scale bars: 1 mm. ( B ) Number of tumors per mouse for WT and S1PR4-KO mice ( n = 9) at day 84 after treatment with AOM/DSS. ( C ) Representative tSNE plots showing the composition of the epithelial layer from WT and S1PR4-KO colons at day 84. ( D and E ) Relative amounts of CD8 + IEL ( D ) and CD8 + Trm IELs ( E ) within the epithelial layer of WT and S1PR4-KO mice at day 0 ( n = 6), day 8 ( n = 8), day 15 ( n = 4), and day 84 ( n = 9) analyzed by flow cytometry. Means ± SEM; 2-tailed Student’s t test; * P
    Figure Legend Snippet: S1PR4 ablation restricts tumor formation of colitis-associated cancer and induces epithelial CD8 + T cell expansion. ( A ) Representative images of WT and S1PR4-KO AOM/DSS-treated colons at day 84 stained with H E. Scale bars: 1 mm. ( B ) Number of tumors per mouse for WT and S1PR4-KO mice ( n = 9) at day 84 after treatment with AOM/DSS. ( C ) Representative tSNE plots showing the composition of the epithelial layer from WT and S1PR4-KO colons at day 84. ( D and E ) Relative amounts of CD8 + IEL ( D ) and CD8 + Trm IELs ( E ) within the epithelial layer of WT and S1PR4-KO mice at day 0 ( n = 6), day 8 ( n = 8), day 15 ( n = 4), and day 84 ( n = 9) analyzed by flow cytometry. Means ± SEM; 2-tailed Student’s t test; * P

    Techniques Used: Staining, Mouse Assay, Flow Cytometry

    21) Product Images from "All-trans Retinoic Acid Counteracts Diarrhea and Inhibition of Downregulated in Adenoma Expression in Gut Inflammation"

    Article Title: All-trans Retinoic Acid Counteracts Diarrhea and Inhibition of Downregulated in Adenoma Expression in Gut Inflammation

    Journal: Inflammatory Bowel Diseases

    doi: 10.1093/ibd/izz249

    All-trans retinoic acid attenuates DSS-induced alterations in body weight and colon weight to length ratio and tissue damage: A, Body weight curves denote the changes in the mean body weight of mice recorded daily for 7 days in different treatment groups (B) representative picture of the colon in control, ATRA-, DSS- and ATRA+DSS-treated mice showing the stool consistency and colon length. C) Colon weight and length (excluding cecum) was recorded for each mice/group on day after harvesting the tissue on day 8. Colon weight to length ratio was calculated for each animal in all the experimental groups. D) Representative image of hematoxylin and eosin staining of colon from control, ATRA-, DSS-, and ATRA+DSS-treated mice. Data are expressed as mean ± SEM for n = 5 mice/group. * P
    Figure Legend Snippet: All-trans retinoic acid attenuates DSS-induced alterations in body weight and colon weight to length ratio and tissue damage: A, Body weight curves denote the changes in the mean body weight of mice recorded daily for 7 days in different treatment groups (B) representative picture of the colon in control, ATRA-, DSS- and ATRA+DSS-treated mice showing the stool consistency and colon length. C) Colon weight and length (excluding cecum) was recorded for each mice/group on day after harvesting the tissue on day 8. Colon weight to length ratio was calculated for each animal in all the experimental groups. D) Representative image of hematoxylin and eosin staining of colon from control, ATRA-, DSS-, and ATRA+DSS-treated mice. Data are expressed as mean ± SEM for n = 5 mice/group. * P

    Techniques Used: Mouse Assay, Staining

    All-trans retinoic acid inhibits DSS-induced decrease in DRA mRNA levels and protein expression in distal colon: A, Total RNA was extracted from the mucosal scrapings of distal colon of control, ATRA, DSS and ATRA+DSS-treated mice. Relative expression of DRA mRNA normalized to GAPDH mRNA (internal control) was assessed by real time RT-PCR. Results are expressed as fold change in mRNA levels compared with control taken as 1.0. B, Protein lysates were prepared from the mucosal scrapings from the distal colon of mice from different treatment groups. Equal amount of protein were separated on a 7.5% SDS-PAGE and electrotransferred to nitrocellulose membrane. The blot was probed with anti-DRA or anti-GAPDH antibody and bands were visualized using Enhanced chemiluminiscence (ECL) solution; i) a representative blot is shown; ii) data were quantified by densitometric analysis and expressed as percentage of control in arbitrary units. C) OCT sections from distal colon of control, ATRA-, DSS-, and ATRA+DSS-treated mice were immunostained for DRA (green), the apical membrane marker Villin (red) and nuclei (blue) as described in Materials and Methods section. A representative image is shown. Scale bar, 20 μm. Data are expressed as mean ± SEM for n = 5 mice/group. * P
    Figure Legend Snippet: All-trans retinoic acid inhibits DSS-induced decrease in DRA mRNA levels and protein expression in distal colon: A, Total RNA was extracted from the mucosal scrapings of distal colon of control, ATRA, DSS and ATRA+DSS-treated mice. Relative expression of DRA mRNA normalized to GAPDH mRNA (internal control) was assessed by real time RT-PCR. Results are expressed as fold change in mRNA levels compared with control taken as 1.0. B, Protein lysates were prepared from the mucosal scrapings from the distal colon of mice from different treatment groups. Equal amount of protein were separated on a 7.5% SDS-PAGE and electrotransferred to nitrocellulose membrane. The blot was probed with anti-DRA or anti-GAPDH antibody and bands were visualized using Enhanced chemiluminiscence (ECL) solution; i) a representative blot is shown; ii) data were quantified by densitometric analysis and expressed as percentage of control in arbitrary units. C) OCT sections from distal colon of control, ATRA-, DSS-, and ATRA+DSS-treated mice were immunostained for DRA (green), the apical membrane marker Villin (red) and nuclei (blue) as described in Materials and Methods section. A representative image is shown. Scale bar, 20 μm. Data are expressed as mean ± SEM for n = 5 mice/group. * P

    Techniques Used: Expressing, Mouse Assay, Quantitative RT-PCR, SDS Page, Marker

    22) Product Images from "Phosphatase Shp2 exacerbates intestinal inflammation by disrupting macrophage responsiveness to interleukin-10"

    Article Title: Phosphatase Shp2 exacerbates intestinal inflammation by disrupting macrophage responsiveness to interleukin-10

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20181198

    Shp2 deficiency in macrophages inhibits colitis-associated colon cancer. (A) Experimental design of AOM/DSS-induced colon cancer. (B) Colonic tumors were photographed (left) and counted (right). n = 9–11. Data are mean ± SEM and are compiled from two independent experiments. (C) Representative H E staining of colon tissues. Bar, 100 µm. (D) The frequencies of different cell populations in CLP were analyzed by flow cytometry. Representative plots showed the myeloid populations. (E) The expression of indicated cytokines in CLP was determined by qPCR. Data are mean ± SEM and are representative of two independent experiments. *, P
    Figure Legend Snippet: Shp2 deficiency in macrophages inhibits colitis-associated colon cancer. (A) Experimental design of AOM/DSS-induced colon cancer. (B) Colonic tumors were photographed (left) and counted (right). n = 9–11. Data are mean ± SEM and are compiled from two independent experiments. (C) Representative H E staining of colon tissues. Bar, 100 µm. (D) The frequencies of different cell populations in CLP were analyzed by flow cytometry. Representative plots showed the myeloid populations. (E) The expression of indicated cytokines in CLP was determined by qPCR. Data are mean ± SEM and are representative of two independent experiments. *, P

    Techniques Used: Staining, Flow Cytometry, Expressing, Real-time Polymerase Chain Reaction

    23) Product Images from "Effect of α4β7 Blockade on Intestinal Lymphocyte Subsets and Lymphoid Tissue Development"

    Article Title: Effect of α4β7 Blockade on Intestinal Lymphocyte Subsets and Lymphoid Tissue Development

    Journal: Inflammatory bowel diseases

    doi: 10.1002/ibd.21266

    Colonic lymphoid aggregates form at the peak of inflammation and persist after colitis resolution. To evaluate the timing of lymphoid aggregate development during acute injury and correlate this with disease progression, Balb/c mice were given 5% DSS
    Figure Legend Snippet: Colonic lymphoid aggregates form at the peak of inflammation and persist after colitis resolution. To evaluate the timing of lymphoid aggregate development during acute injury and correlate this with disease progression, Balb/c mice were given 5% DSS

    Techniques Used: Mouse Assay

    24) Product Images from "RNase-L deficiency exacerbates experimental colitis and colitis-associated cancer"

    Article Title: RNase-L deficiency exacerbates experimental colitis and colitis-associated cancer

    Journal: Inflammatory bowel diseases

    doi: 10.1097/MIB.0b013e318281f2fd

    RNase-L promotes an early inflammatory response resulting in attenuated tissue damage in WT mice. H E-stained colon sections were prepared from DSS-treated mice for histological analysis. Samples from days 0, 5 (n = 6) and 9 (n = 7) were analyzed.
    Figure Legend Snippet: RNase-L promotes an early inflammatory response resulting in attenuated tissue damage in WT mice. H E-stained colon sections were prepared from DSS-treated mice for histological analysis. Samples from days 0, 5 (n = 6) and 9 (n = 7) were analyzed.

    Techniques Used: Mouse Assay, Staining

    RNase-L influences immune cell infiltration during experimental colitis. Colon from DSS-treated mice was utilized for immunohistochemistry for immune cell markers. Day 7 frozen colon tissue was stained with antibody to (A) F4/80, (B) 33D1, (C) CD3 and
    Figure Legend Snippet: RNase-L influences immune cell infiltration during experimental colitis. Colon from DSS-treated mice was utilized for immunohistochemistry for immune cell markers. Day 7 frozen colon tissue was stained with antibody to (A) F4/80, (B) 33D1, (C) CD3 and

    Techniques Used: Mouse Assay, Immunohistochemistry, Staining

    RNase-L is required for optimal induction of cytokine expression following DSS-induced damage. Colon tissue collected from DSS-treated mice at days 5 and 9 (n = 6) was analyzed by qRT-PCR for the expression of (A) IFNβ, (B) IL-1β, (C)
    Figure Legend Snippet: RNase-L is required for optimal induction of cytokine expression following DSS-induced damage. Colon tissue collected from DSS-treated mice at days 5 and 9 (n = 6) was analyzed by qRT-PCR for the expression of (A) IFNβ, (B) IL-1β, (C)

    Techniques Used: Expressing, Mouse Assay, Quantitative RT-PCR

    RNase-L is protective against DSS-induced colitis and promotes recovery following GI injury. RNase-L −/− and WT mice were treated with 2.5% DSS w/v drinking water or regular water control for 9 days. Mice were euthanized at days 0, 1, 3,
    Figure Legend Snippet: RNase-L is protective against DSS-induced colitis and promotes recovery following GI injury. RNase-L −/− and WT mice were treated with 2.5% DSS w/v drinking water or regular water control for 9 days. Mice were euthanized at days 0, 1, 3,

    Techniques Used: Mouse Assay

    25) Product Images from "Inflammation-induced tumorigenesis in the colon is regulated by caspase-1 and NLRC4"

    Article Title: Inflammation-induced tumorigenesis in the colon is regulated by caspase-1 and NLRC4

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.1016814108

    No differences in inflammation between WT and Casp1 −/− mice during acute DSS colitis. There were no significant difference in percent-mass change ( A ), colonoscopy inflammation severity score ( B ), severity of histopathological morphology ( C ) (H E staining), or histopathology parameters for edema, inflammation, ulceration or overall severity of injury ( D ) between WT and Casp1 −/− mice. (Scale bars in C , 200 μm.) ( E ) Likewise, the severity of chronic DSS colitis was similar between WT and Casp1 −/− mice. All experiments were repeated twice.
    Figure Legend Snippet: No differences in inflammation between WT and Casp1 −/− mice during acute DSS colitis. There were no significant difference in percent-mass change ( A ), colonoscopy inflammation severity score ( B ), severity of histopathological morphology ( C ) (H E staining), or histopathology parameters for edema, inflammation, ulceration or overall severity of injury ( D ) between WT and Casp1 −/− mice. (Scale bars in C , 200 μm.) ( E ) Likewise, the severity of chronic DSS colitis was similar between WT and Casp1 −/− mice. All experiments were repeated twice.

    Techniques Used: Mouse Assay, Staining, Histopathology

    Enhanced colon epithelial and tumor cell proliferation in Casp1 −/− mice during inflammation-induced colorectal cancer. Representative H E, Ki67, and BrdU immunohistochemistry at day 15 ( A–F ) and at day 65 ( G–I ), and TUNEL-positive cells in colons (day 8) and tumors (day 65) in WT and Casp1 −/− mice given AOM-DSS. The majority of crypts at day 15 appeared normal ( A ); however, there were increased Ki67 + ( B ) and BrdU + ( C ) crypt epithelial cells in Casp1 −/− mice compared with WT mice. In foci of crypt hyperplasia/dysplasia ( D ), there were no significant difference in the number of Ki6 + cells ( E ) and a moderate increase in the number of BrdU + cells ( F ) in Casp1 −/− compared with WT mice. At day 65 there were numerous large colon adenocarcinomas ( G ) with increased numbers of Ki67 + tumor cells ( H ) and BrdU + tumor cells ( I ) in Casp1 −/− compared with WT mice. ( A , D , G : H E staining; B , C , E , F , H , and I : DAB, Hematoxalyn) (Scale bars, 200 μm). ( J ) The number of TUNEL-positive cells in colon is similar in WT compared with Casp1 −/− mice. In contrast, there is reduced cell death of tumor tissue in Casp1 −/− mice (average cells counted: WT: 34.27 ± 8.964 positive cells/293.6 ± 86.39 total cells per field; Casp1 −/− : 16.87 ± 4.533 positive cells/364.2 ± 98.70 total cells per field). DNA fragmentation in WT and Casp-1 −/− mice was determined on either whole-colon sections on day 8 of AOM-DSS model or tumor tissues at day 65. Error bars represent ± SEM, P
    Figure Legend Snippet: Enhanced colon epithelial and tumor cell proliferation in Casp1 −/− mice during inflammation-induced colorectal cancer. Representative H E, Ki67, and BrdU immunohistochemistry at day 15 ( A–F ) and at day 65 ( G–I ), and TUNEL-positive cells in colons (day 8) and tumors (day 65) in WT and Casp1 −/− mice given AOM-DSS. The majority of crypts at day 15 appeared normal ( A ); however, there were increased Ki67 + ( B ) and BrdU + ( C ) crypt epithelial cells in Casp1 −/− mice compared with WT mice. In foci of crypt hyperplasia/dysplasia ( D ), there were no significant difference in the number of Ki6 + cells ( E ) and a moderate increase in the number of BrdU + cells ( F ) in Casp1 −/− compared with WT mice. At day 65 there were numerous large colon adenocarcinomas ( G ) with increased numbers of Ki67 + tumor cells ( H ) and BrdU + tumor cells ( I ) in Casp1 −/− compared with WT mice. ( A , D , G : H E staining; B , C , E , F , H , and I : DAB, Hematoxalyn) (Scale bars, 200 μm). ( J ) The number of TUNEL-positive cells in colon is similar in WT compared with Casp1 −/− mice. In contrast, there is reduced cell death of tumor tissue in Casp1 −/− mice (average cells counted: WT: 34.27 ± 8.964 positive cells/293.6 ± 86.39 total cells per field; Casp1 −/− : 16.87 ± 4.533 positive cells/364.2 ± 98.70 total cells per field). DNA fragmentation in WT and Casp-1 −/− mice was determined on either whole-colon sections on day 8 of AOM-DSS model or tumor tissues at day 65. Error bars represent ± SEM, P

    Techniques Used: Mouse Assay, Immunohistochemistry, TUNEL Assay, Staining

    26) Product Images from "Peptidoglycan recognition protein 3 and Nod2 synergistically protect mice from dextran sodium sulfate-induced colitis"

    Article Title: Peptidoglycan recognition protein 3 and Nod2 synergistically protect mice from dextran sodium sulfate-induced colitis

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1301548

    Pglyrp3 −/− Nod2 −/− mice express higher levels of chemokine and cytokine mRNA in the colon following DSS treatment
    Figure Legend Snippet: Pglyrp3 −/− Nod2 −/− mice express higher levels of chemokine and cytokine mRNA in the colon following DSS treatment

    Techniques Used: Mouse Assay

    Pglyrp3 −/− Nod2 −/− and Pglyrp3 −/− mice have higher levels of ATP in the colon, and intestinal ATP preferentially increases sensitivity of Nod2 −/− mice to DSS-colitis
    Figure Legend Snippet: Pglyrp3 −/− Nod2 −/− and Pglyrp3 −/− mice have higher levels of ATP in the colon, and intestinal ATP preferentially increases sensitivity of Nod2 −/− mice to DSS-colitis

    Techniques Used: Mouse Assay

    Pglyrp3 −/− Nod2 −/− mice are more susceptible to DSS-induced colitis than Pglyrp3 and Nod2 single-deficient mice
    Figure Legend Snippet: Pglyrp3 −/− Nod2 −/− mice are more susceptible to DSS-induced colitis than Pglyrp3 and Nod2 single-deficient mice

    Techniques Used: Mouse Assay

    27) Product Images from "Cohousing-mediated microbiota transfer from milk bioactive components-dosed mice ameliorate colitis by remodeling colonic mucus barrier and lamina propria macrophages"

    Article Title: Cohousing-mediated microbiota transfer from milk bioactive components-dosed mice ameliorate colitis by remodeling colonic mucus barrier and lamina propria macrophages

    Journal: Gut Microbes

    doi: 10.1080/19490976.2021.1903826

    RNA-seq data exhibit distinct colonic function in colonic tissues. A) Heatmap summary of the differentially expressed genes. The scale bar shows the gene expression in each group. B) Volcano plot of differentially expressed transcripts with DSS and CMFG + DSS groups. C) GO enrichment of up-regulated and down-regulated genes in DSS vs. CMFG + DSS. D) KEGG enrichment of up-regulated and down-regulated genes in DSS vs. CMFG + DSS, n = 5 per group
    Figure Legend Snippet: RNA-seq data exhibit distinct colonic function in colonic tissues. A) Heatmap summary of the differentially expressed genes. The scale bar shows the gene expression in each group. B) Volcano plot of differentially expressed transcripts with DSS and CMFG + DSS groups. C) GO enrichment of up-regulated and down-regulated genes in DSS vs. CMFG + DSS. D) KEGG enrichment of up-regulated and down-regulated genes in DSS vs. CMFG + DSS, n = 5 per group

    Techniques Used: RNA Sequencing Assay, Expressing

    Cohousing of CMFG-dosed mice prevents acute DSS colitis. A) experimental strategy, B) DAI score, C) body weight change, D) colon length, E) representative picture of the colon, F) summarized histological score, G) H E staining of the colon, H) Alican Blue staining, I) PAS staining, J) representative pictures of transmission electron microscopy. IL-1β (k), IL-6 (l), IFN-γ (m), TNF-α (n), T-SOD (o), MDA (p) level in the plasma. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Cohousing of CMFG-dosed mice prevents acute DSS colitis. A) experimental strategy, B) DAI score, C) body weight change, D) colon length, E) representative picture of the colon, F) summarized histological score, G) H E staining of the colon, H) Alican Blue staining, I) PAS staining, J) representative pictures of transmission electron microscopy. IL-1β (k), IL-6 (l), IFN-γ (m), TNF-α (n), T-SOD (o), MDA (p) level in the plasma. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM

    Techniques Used: Mouse Assay, Staining, Transmission Assay, Electron Microscopy, Multiple Displacement Amplification

    Prophylactic CMFG intervention alters the levels of cellular proliferation and apoptosis. Representative plot of cellular proliferation (a) and cellular apoptosis (b) in the colonic tissues among vehicle, DSS and CMFG + DSS groups. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Prophylactic CMFG intervention alters the levels of cellular proliferation and apoptosis. Representative plot of cellular proliferation (a) and cellular apoptosis (b) in the colonic tissues among vehicle, DSS and CMFG + DSS groups. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM

    Techniques Used:

    Cohousing of CMFG-dosed mice altered the frequency of colon-infiltrating immune cells in colonic tissues. Representative plot of DC cells (a), Macrophages (b), Neutrophils (c), NK cells (d), and Treg cells (e) in the colonic tissues among DSS, CMFG + DSS, vehicle-cohousing + DSS group and CMFG-cohousing + DSS. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Cohousing of CMFG-dosed mice altered the frequency of colon-infiltrating immune cells in colonic tissues. Representative plot of DC cells (a), Macrophages (b), Neutrophils (c), NK cells (d), and Treg cells (e) in the colonic tissues among DSS, CMFG + DSS, vehicle-cohousing + DSS group and CMFG-cohousing + DSS. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM

    Techniques Used: Mouse Assay

    Prophylactic CMFG intervention prevents acute DSS colitis. A) experimental strategy, B) DAI score, C) body weight change, D) colon length, E) representative picture of the colon, F) summarized histological score, G) H E staining of the colon, H) Alican blue staining, I) PAS staining, J) representative pictures of transmission electron microscopy. IL-1β (k), IL-6 (l), IFN-γ (m), TNF-α (n), T-SOD (o), MDA (p) level in the plasma. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Prophylactic CMFG intervention prevents acute DSS colitis. A) experimental strategy, B) DAI score, C) body weight change, D) colon length, E) representative picture of the colon, F) summarized histological score, G) H E staining of the colon, H) Alican blue staining, I) PAS staining, J) representative pictures of transmission electron microscopy. IL-1β (k), IL-6 (l), IFN-γ (m), TNF-α (n), T-SOD (o), MDA (p) level in the plasma. Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM

    Techniques Used: Staining, Transmission Assay, Electron Microscopy, Multiple Displacement Amplification

    Prophylactic CMFG intervention altered the frequency of colon-infiltrating immune cells in colonic tissues. Representative plot of DC cells (a), Macrophages (b), Neutrophils (c), NK cells (d), and Treg cells (e) in the colonic tissues from DSS and CMFG + DSS groups. Asterisks denote significant differences (* p ≤ 0.05), n = 4 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Prophylactic CMFG intervention altered the frequency of colon-infiltrating immune cells in colonic tissues. Representative plot of DC cells (a), Macrophages (b), Neutrophils (c), NK cells (d), and Treg cells (e) in the colonic tissues from DSS and CMFG + DSS groups. Asterisks denote significant differences (* p ≤ 0.05), n = 4 per group, data are represented as mean ± SEM

    Techniques Used:

    Cohousing of CMFG-dosed mice alters the levels of cellular proliferation and apoptosis. Representative plot of cellular proliferation (a) and cellular apoptosis (b) in the colonic tissues among DSS, CMFG + DSS, vehicle-cohousing + DSS group and CMFG-cohousing + DSS. Asterisks denote significant differences (* p ≤ 0.05, *** p ≤ 0.001), n = 5 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Cohousing of CMFG-dosed mice alters the levels of cellular proliferation and apoptosis. Representative plot of cellular proliferation (a) and cellular apoptosis (b) in the colonic tissues among DSS, CMFG + DSS, vehicle-cohousing + DSS group and CMFG-cohousing + DSS. Asterisks denote significant differences (* p ≤ 0.05, *** p ≤ 0.001), n = 5 per group, data are represented as mean ± SEM

    Techniques Used: Mouse Assay

    Prophylactic CMFG intervention alters the gut microbial composition and SCFAs production. A) Shannon index of OTU level. B) Sobs index of OTU level. C-E) PCoA plots assessed by Adonis analysis among these groups at day 0, at day 3, and at day 7, respectively. F) shows the relative abundance of microbial OTUs, classified at the phylum and genus level, in different groups. Linear discriminate analysis effect size (LEfSe) was performed to determine the difference in abundance at day 0 (g), day 3 (h), and at day 7 (i). SCFAs concentrations from feces among Vehicle, DSS, and CMFG + DSS groups are shown in J (acetate), K (propionate) and L (butyrate). Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM
    Figure Legend Snippet: Prophylactic CMFG intervention alters the gut microbial composition and SCFAs production. A) Shannon index of OTU level. B) Sobs index of OTU level. C-E) PCoA plots assessed by Adonis analysis among these groups at day 0, at day 3, and at day 7, respectively. F) shows the relative abundance of microbial OTUs, classified at the phylum and genus level, in different groups. Linear discriminate analysis effect size (LEfSe) was performed to determine the difference in abundance at day 0 (g), day 3 (h), and at day 7 (i). SCFAs concentrations from feces among Vehicle, DSS, and CMFG + DSS groups are shown in J (acetate), K (propionate) and L (butyrate). Asterisks denote significant differences (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001), n = 6 per group, data are represented as mean ± SEM

    Techniques Used:

    28) Product Images from "Hypoxia inducible factor‐1α‐induced interleukin‐33 expression in intestinal epithelia contributes to mucosal homeostasis in inflammatory bowel disease"

    Article Title: Hypoxia inducible factor‐1α‐induced interleukin‐33 expression in intestinal epithelia contributes to mucosal homeostasis in inflammatory bowel disease

    Journal: Clinical and Experimental Immunology

    doi: 10.1111/cei.12896

    Hypoxia inducible factor‐1α (HIF‐1α) promotes interleukin (IL)−33 expression in inflamed colon of mice with dextran sulphate sodium (DSS)‐induced colitis. (a) Six to 8‐week‐old C57BL/B6 mice (10 mice per group) were given 2% DSS in drinking water for 7 days, and switched to drinking water for an additional 3 days. Haematoxylin and eosin (H E) staining in colonic tissues from wild‐type (WT) and DSS‐treated mice. (b−e) Quantitative real‐time–polymerase chain reaction (qRT–PCR) analysis for tumour necrosis factor (TNF), HIF‐1α, IL‐33 and vascular endothelial growth factor (VEGF) in colonic tissues of WT and DSS‐treated mice. Glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) was used as a housekeeping gene. * P
    Figure Legend Snippet: Hypoxia inducible factor‐1α (HIF‐1α) promotes interleukin (IL)−33 expression in inflamed colon of mice with dextran sulphate sodium (DSS)‐induced colitis. (a) Six to 8‐week‐old C57BL/B6 mice (10 mice per group) were given 2% DSS in drinking water for 7 days, and switched to drinking water for an additional 3 days. Haematoxylin and eosin (H E) staining in colonic tissues from wild‐type (WT) and DSS‐treated mice. (b−e) Quantitative real‐time–polymerase chain reaction (qRT–PCR) analysis for tumour necrosis factor (TNF), HIF‐1α, IL‐33 and vascular endothelial growth factor (VEGF) in colonic tissues of WT and DSS‐treated mice. Glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) was used as a housekeeping gene. * P

    Techniques Used: Expressing, Mouse Assay, Staining, Real-time Polymerase Chain Reaction, Quantitative RT-PCR

    29) Product Images from "Translocation of Viable Gut Microbiota to Mesenteric Adipose Drives Formation of Creeping Fat in Humans"

    Article Title: Translocation of Viable Gut Microbiota to Mesenteric Adipose Drives Formation of Creeping Fat in Humans

    Journal: Cell

    doi: 10.1016/j.cell.2020.09.009

    C. innocuum Translocation Promotes MAT Expansion and Attenuated Systemic Dissemination of Bacterial LPS (A) Gut barrier gene expression measured by qRT-PCR in CD, UC, and H MUC. Data below the dotted line represent downregulation of target genes compared to H MUC (H MUC, n = 4; CD, n = 10; UC, n = 8). (B) Plasma LBP and soluble CD14 from the same CD and UC as in (A). Healthy samples are a combination of H patients in (A) (open symbols) and ten additional healthy blood donors (H, n = 14; CD, n = 14; UC, n = 11). (C) Representative images of ileal-mesenteric region in ASF gnotobiotic mice gavaged with the following: PBS (left), live C. innocuum (middle), and live C. innocuum + DSS (right). Black arrow points to the MAT. (D) Gnotobiotic mice body weight change compared to baseline. Untreated, n = 3; C. innocuum alone, n = 2; C. innocuum + DSS, n = 2. (E) Colon lengths. (F) Translocated bacteria recovered from MAT of mice from (C). Arrows indicate distinct bacterial species (representative isolates; yellow, ASF; blue, C. innocuum ). (G) qRT-PCR of adipogenesis and ECM markers in gnotobiotic MAT. (H) Endpoint plasma LBP in gnotobiotic mice. Error bars ± SEM. One-way ANOVA with Tukey’s multiple comparison test. ∗ p
    Figure Legend Snippet: C. innocuum Translocation Promotes MAT Expansion and Attenuated Systemic Dissemination of Bacterial LPS (A) Gut barrier gene expression measured by qRT-PCR in CD, UC, and H MUC. Data below the dotted line represent downregulation of target genes compared to H MUC (H MUC, n = 4; CD, n = 10; UC, n = 8). (B) Plasma LBP and soluble CD14 from the same CD and UC as in (A). Healthy samples are a combination of H patients in (A) (open symbols) and ten additional healthy blood donors (H, n = 14; CD, n = 14; UC, n = 11). (C) Representative images of ileal-mesenteric region in ASF gnotobiotic mice gavaged with the following: PBS (left), live C. innocuum (middle), and live C. innocuum + DSS (right). Black arrow points to the MAT. (D) Gnotobiotic mice body weight change compared to baseline. Untreated, n = 3; C. innocuum alone, n = 2; C. innocuum + DSS, n = 2. (E) Colon lengths. (F) Translocated bacteria recovered from MAT of mice from (C). Arrows indicate distinct bacterial species (representative isolates; yellow, ASF; blue, C. innocuum ). (G) qRT-PCR of adipogenesis and ECM markers in gnotobiotic MAT. (H) Endpoint plasma LBP in gnotobiotic mice. Error bars ± SEM. One-way ANOVA with Tukey’s multiple comparison test. ∗ p

    Techniques Used: Translocation Assay, Expressing, Quantitative RT-PCR, Mouse Assay

    30) Product Images from "Tracing the origin of adult intestinal stem cells"

    Article Title: Tracing the origin of adult intestinal stem cells

    Journal: Nature

    doi: 10.1038/s41586-019-1212-5

    Testing intestinal epithelial cells for equipotency. a) Detection of Lgr5-eGFP (green) and CD44 (red) in the E16.5 small intestine isolated from Lgr5-eGFP-ires-CreER T2 E16.5 animals. Tissue was counterstained with DAPI (blue). Samples from 3 animals were analyzed and a representative image is shown Scale bars: 50μm. b) Cartoon depicting the positions used to quantify the pattern of CD44 and Lgr5 expression. Quantifications of the localization of CD44 and Lgr5 positive cells. A total of 14 intervillus regions (x-axis) were quantified up to position +/- 10 (y-axis). c-d) Representative FACS dot plot illustrating the gating strategy used to quantify CD44. Dots represent the quantification in individual animals (n=4). e) Spheroids forming from cells isolated based on DAPI neg EpCAM pos Lgr5-eGFP pos and DAPI neg EpCAM pos Lgr5-eGFP neg from the proximal half of the small intestine from mice at E16.5. Representative pictures of n=3 biologically independent samples. f) Quantification of spheroid seeding efficiency following isolation based on either CD44 or Lgr5 (n=3 animals per condition). g-i) Gating strategy for purification of villus and intervillus cells for transplantation. The gating hierarchy of the panels is number i-vi (g), example of purity is indicated (h), mT/mG derived organoid is shown in (i). Spheroids were generated from a pool of n=6 biologically independent samples. j-k) Outline for transplantation experiment. Briefly, experimental colitis was induced in RAG2 -/- animals by administration of DSS in the drinking water. Organoids from the different cultures were subsequently infused into lumen of the animals (j) and engrafted regions were immunostained for lineage and stem cell markers depicted (k). l) Scheme summarizing the main findings of this work.
    Figure Legend Snippet: Testing intestinal epithelial cells for equipotency. a) Detection of Lgr5-eGFP (green) and CD44 (red) in the E16.5 small intestine isolated from Lgr5-eGFP-ires-CreER T2 E16.5 animals. Tissue was counterstained with DAPI (blue). Samples from 3 animals were analyzed and a representative image is shown Scale bars: 50μm. b) Cartoon depicting the positions used to quantify the pattern of CD44 and Lgr5 expression. Quantifications of the localization of CD44 and Lgr5 positive cells. A total of 14 intervillus regions (x-axis) were quantified up to position +/- 10 (y-axis). c-d) Representative FACS dot plot illustrating the gating strategy used to quantify CD44. Dots represent the quantification in individual animals (n=4). e) Spheroids forming from cells isolated based on DAPI neg EpCAM pos Lgr5-eGFP pos and DAPI neg EpCAM pos Lgr5-eGFP neg from the proximal half of the small intestine from mice at E16.5. Representative pictures of n=3 biologically independent samples. f) Quantification of spheroid seeding efficiency following isolation based on either CD44 or Lgr5 (n=3 animals per condition). g-i) Gating strategy for purification of villus and intervillus cells for transplantation. The gating hierarchy of the panels is number i-vi (g), example of purity is indicated (h), mT/mG derived organoid is shown in (i). Spheroids were generated from a pool of n=6 biologically independent samples. j-k) Outline for transplantation experiment. Briefly, experimental colitis was induced in RAG2 -/- animals by administration of DSS in the drinking water. Organoids from the different cultures were subsequently infused into lumen of the animals (j) and engrafted regions were immunostained for lineage and stem cell markers depicted (k). l) Scheme summarizing the main findings of this work.

    Techniques Used: Isolation, Expressing, FACS, Mouse Assay, Purification, Transplantation Assay, Derivative Assay, Generated

    31) Product Images from "VEGFR-3 blocking deteriorates inflammation with impaired lymphatic function and different changes in lymphatic vessels in acute and chronic colitis"

    Article Title: VEGFR-3 blocking deteriorates inflammation with impaired lymphatic function and different changes in lymphatic vessels in acute and chronic colitis

    Journal: American Journal of Translational Research

    doi:

    Blocking VEGFR-3 exacerbates colon inflammation in acute and chronic colitis. C57BL/6 mice fed with 5% DSS for 7 days to induce acute colitis were treated intraperitoneally with anti-VEGFR-3 antibody once daily ( n = 5/group). Anti-VEGFR-3 antibody treatment
    Figure Legend Snippet: Blocking VEGFR-3 exacerbates colon inflammation in acute and chronic colitis. C57BL/6 mice fed with 5% DSS for 7 days to induce acute colitis were treated intraperitoneally with anti-VEGFR-3 antibody once daily ( n = 5/group). Anti-VEGFR-3 antibody treatment

    Techniques Used: Blocking Assay, Mouse Assay

    32) Product Images from "Dietary phenethylisothiocyanate attenuates bowel inflammation in mice"

    Article Title: Dietary phenethylisothiocyanate attenuates bowel inflammation in mice

    Journal: BMC Chemical Biology

    doi: 10.1186/1472-6769-10-4

    Effects of orally administered PEO and 5-ASA on colon length and histopathology . Experimental groups (chronic) and disease induction are defined in Table 1. (A) The DSS receiving groups had shorter average colon length as compared to water group (healthy controls) (n = 10). The shortening was relieved significantly in PEO treated group with respect to DSS group (*, p
    Figure Legend Snippet: Effects of orally administered PEO and 5-ASA on colon length and histopathology . Experimental groups (chronic) and disease induction are defined in Table 1. (A) The DSS receiving groups had shorter average colon length as compared to water group (healthy controls) (n = 10). The shortening was relieved significantly in PEO treated group with respect to DSS group (*, p

    Techniques Used: Histopathology

    Effects of orally administered PEO and 5-ASA on the Disease activity index (DAI) in DSS-induced colitis . Experimental mouse groups and disease induction are defined in Table 1 and scoring criteria in Table 2. Significance of treatments in PEO and 5-ASA groups in respect to DSS group and are indicated by *, p
    Figure Legend Snippet: Effects of orally administered PEO and 5-ASA on the Disease activity index (DAI) in DSS-induced colitis . Experimental mouse groups and disease induction are defined in Table 1 and scoring criteria in Table 2. Significance of treatments in PEO and 5-ASA groups in respect to DSS group and are indicated by *, p

    Techniques Used: Activity Assay

    33) Product Images from "Knockdown of IGF-1R Triggers Viral RNA Sensor MDA5- and RIG-I-Mediated Mitochondrial Apoptosis in Colonic Cancer Cells"

    Article Title: Knockdown of IGF-1R Triggers Viral RNA Sensor MDA5- and RIG-I-Mediated Mitochondrial Apoptosis in Colonic Cancer Cells

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2019.02.008

    IGF-1R Knockdown-Triggered MDA5 and RIG-I Mediated Mitochondrial Apoptosis, Leading to Cancer Inhibition in Igf1r +/− Mice Igf1r +/− mice and their WT littermates were exposed to AOM-DSS for inducing colorectal cancer. (A) Igf1r +/− mice had higher MDA5 and RIG-I levels in the colorectal epithelium than WT mice. (B) Igf1r +/− mice developed less colorectal tumor than WT mice (left), showing decreased incidence (middle) and size of tumor (right). (C) Histopathological analyses showed advanced adenocarcinoma in WT mice, while only low-grade dysplastic mucosa appeared in Igf1r +/− mice. (D) IHC analysis showed a strong diffuse staining of Ki-67 and PCNA in the colorectal cancer of WT mice, whereas it showed only scattered positivity in the basal cells of colorectal crypt in Igf1r +/− mice. (E) TUNEL staining analysis showed increased apoptotic epithelium in Igf1r +/− mice. (F) Western blotting analysis showed increased Bim and apoptosome (cytochrome c , apoptotic peptidase-activating factor 1 [Apaf-1], and caspase-9 and caspase-3) in colorectal epithelium of Igf1r +/− mice (n = 6). *p
    Figure Legend Snippet: IGF-1R Knockdown-Triggered MDA5 and RIG-I Mediated Mitochondrial Apoptosis, Leading to Cancer Inhibition in Igf1r +/− Mice Igf1r +/− mice and their WT littermates were exposed to AOM-DSS for inducing colorectal cancer. (A) Igf1r +/− mice had higher MDA5 and RIG-I levels in the colorectal epithelium than WT mice. (B) Igf1r +/− mice developed less colorectal tumor than WT mice (left), showing decreased incidence (middle) and size of tumor (right). (C) Histopathological analyses showed advanced adenocarcinoma in WT mice, while only low-grade dysplastic mucosa appeared in Igf1r +/− mice. (D) IHC analysis showed a strong diffuse staining of Ki-67 and PCNA in the colorectal cancer of WT mice, whereas it showed only scattered positivity in the basal cells of colorectal crypt in Igf1r +/− mice. (E) TUNEL staining analysis showed increased apoptotic epithelium in Igf1r +/− mice. (F) Western blotting analysis showed increased Bim and apoptosome (cytochrome c , apoptotic peptidase-activating factor 1 [Apaf-1], and caspase-9 and caspase-3) in colorectal epithelium of Igf1r +/− mice (n = 6). *p

    Techniques Used: Inhibition, Mouse Assay, Immunohistochemistry, Staining, TUNEL Assay, Western Blot

    34) Product Images from "Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis"

    Article Title: Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.584508

    CHL1 deficiency exacerbated epithelial barrier damage in inflammatory bowel disease (IBD). (A) High magnification histological images of colonic tissue from CHL1 +/+ and CHL1 −/− mice with and without DSS treatment showed altered intestinal epithelial cellular shape in tissues from CHL1 −/− animals. Insets show examples of areas of the epithelium under ultrahigh magnification. (B) Intestinal permeability was measured by the appearance of orally administered FITC-labeled dextran in the serum of DSS-exposed CHL1 +/+ and CHL1 −/− mice ( *** p
    Figure Legend Snippet: CHL1 deficiency exacerbated epithelial barrier damage in inflammatory bowel disease (IBD). (A) High magnification histological images of colonic tissue from CHL1 +/+ and CHL1 −/− mice with and without DSS treatment showed altered intestinal epithelial cellular shape in tissues from CHL1 −/− animals. Insets show examples of areas of the epithelium under ultrahigh magnification. (B) Intestinal permeability was measured by the appearance of orally administered FITC-labeled dextran in the serum of DSS-exposed CHL1 +/+ and CHL1 −/− mice ( *** p

    Techniques Used: Mouse Assay, Permeability, Labeling

    CHL1 deficiency induced inflammatory cell infiltration (A,B) Representative immunohistochemical images (A) and analysis (B) of Ly6B.2-stained colon tissue from DSS-exposed CHL1 +/+ and CHL1 −/− mice ( * p
    Figure Legend Snippet: CHL1 deficiency induced inflammatory cell infiltration (A,B) Representative immunohistochemical images (A) and analysis (B) of Ly6B.2-stained colon tissue from DSS-exposed CHL1 +/+ and CHL1 −/− mice ( * p

    Techniques Used: Immunohistochemistry, Staining, Mouse Assay

    Model of CHL1 deficiency-mediated exacerbation in mouse colitis. The loss of CHL1 exacerbates DSS-induced intestinal inflammation and immune responses in mice. Lamina propria is edematous. Inflammation cells, such as neutrophils and macrophages, infiltrate epithelial layer cell. CHL1 deficiency damages intestinal epithelial cells, and leads to the injury of epithelial barrier function. Furthermore, FITC cross the epithelial barrier after DSS exposure in CHL1 −/− mice.
    Figure Legend Snippet: Model of CHL1 deficiency-mediated exacerbation in mouse colitis. The loss of CHL1 exacerbates DSS-induced intestinal inflammation and immune responses in mice. Lamina propria is edematous. Inflammation cells, such as neutrophils and macrophages, infiltrate epithelial layer cell. CHL1 deficiency damages intestinal epithelial cells, and leads to the injury of epithelial barrier function. Furthermore, FITC cross the epithelial barrier after DSS exposure in CHL1 −/− mice.

    Techniques Used: Mouse Assay

    CHL1 expression was increased in dextran sulfate sodium (DSS)-induced colitis. (A) DSS-induced acute colitis mouse model. CHL1 +/+ mice had ad libitum access to sterile drinking water containing 2.2% DSS for 7 days, followed by normal drinking water for 2 days. The mice were euthanized on the 5th, 7th, and 9th days after the initiation of DSS treatment. (B) Body weight loss in the DSS-induced acute colitis mouse model ( * p
    Figure Legend Snippet: CHL1 expression was increased in dextran sulfate sodium (DSS)-induced colitis. (A) DSS-induced acute colitis mouse model. CHL1 +/+ mice had ad libitum access to sterile drinking water containing 2.2% DSS for 7 days, followed by normal drinking water for 2 days. The mice were euthanized on the 5th, 7th, and 9th days after the initiation of DSS treatment. (B) Body weight loss in the DSS-induced acute colitis mouse model ( * p

    Techniques Used: Expressing, Mouse Assay

    (Continued)FIGURE 2CHL1 deficiency augmented DSS-induced colitis in mice. (A) DSS-induced acute colitis mouse model. CHL1 +/+ , CHL1 +/− , and CHL1 −/− mice had ad libitum access to sterile drinking water containing 1.5% DSS for 7 days, followed by normal drinking water for 2 days. The mice were euthanized on the 9th day after the initiation of DSS treatment. (B,C) Body weight loss and the disease activity index score in DSS-exposed CHL1 +/+ , CHL1 +/− , and CHL1 −/− mice (DSS-induced CHL1 +/+ group vs. DSS-induced CHL1 +/− group, *** p
    Figure Legend Snippet: (Continued)FIGURE 2CHL1 deficiency augmented DSS-induced colitis in mice. (A) DSS-induced acute colitis mouse model. CHL1 +/+ , CHL1 +/− , and CHL1 −/− mice had ad libitum access to sterile drinking water containing 1.5% DSS for 7 days, followed by normal drinking water for 2 days. The mice were euthanized on the 9th day after the initiation of DSS treatment. (B,C) Body weight loss and the disease activity index score in DSS-exposed CHL1 +/+ , CHL1 +/− , and CHL1 −/− mice (DSS-induced CHL1 +/+ group vs. DSS-induced CHL1 +/− group, *** p

    Techniques Used: Mouse Assay, Activity Assay

    35) Product Images from "Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression"

    Article Title: Long non-coding RNA growth arrest specific transcript 5 acts as a tumour suppressor in colorectal cancer by inhibiting interleukin-10 and vascular endothelial growth factor expression

    Journal: Oncotarget

    doi: 10.18632/oncotarget.14625

    Correlations of GAS5 levels with IL-10, VEGF-A and TNF-α in colorectal tumour tissues and GAS5 downregulation in the CAC mouse model ( A–C ) The RNA levels were determined by RT-qPCR relative to GAPDH. A significant negative correlation was observed between GAS5 expression and mRNA levels of IL-10, VEGF-A and TNF-α in CRC samples (n = 24). The r values and P values are from Pearson's correlation analysis. ( D ) Diagram of AOM/DSS administration schedule for establishing the colitis-associated colon cancer model. ( E ) GAS5 downregulation in the colon of wild type (WT) mice on day 71 of AOM/DSS administration compared with the control group ( n = 10). The results are shown as the mean ± SEM relative to GAPDH levels from three experiments. * P
    Figure Legend Snippet: Correlations of GAS5 levels with IL-10, VEGF-A and TNF-α in colorectal tumour tissues and GAS5 downregulation in the CAC mouse model ( A–C ) The RNA levels were determined by RT-qPCR relative to GAPDH. A significant negative correlation was observed between GAS5 expression and mRNA levels of IL-10, VEGF-A and TNF-α in CRC samples (n = 24). The r values and P values are from Pearson's correlation analysis. ( D ) Diagram of AOM/DSS administration schedule for establishing the colitis-associated colon cancer model. ( E ) GAS5 downregulation in the colon of wild type (WT) mice on day 71 of AOM/DSS administration compared with the control group ( n = 10). The results are shown as the mean ± SEM relative to GAPDH levels from three experiments. * P

    Techniques Used: Quantitative RT-PCR, Expressing, Mouse Assay

    36) Product Images from "Expression profile of intestinal stem cell markers in colitis-associated carcinogenesis"

    Article Title: Expression profile of intestinal stem cell markers in colitis-associated carcinogenesis

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-06900-x

    Expression of tuft cell and progenitor cell markers in colitis-associated carcinogenesis (CAC). ( A ) Diagram of tuft cell and progenitor cell markers in the crypt. ( B and C ) Real-time PCR analysis of tuft cell marker Dclk1 and progenitor cell markers Prom1, Ephb2, and Msi1. Data represent the means ± SEM. (DSS: n = 4, AOM/DSS: n = 5). ( D ) Relative mRNA expression of ISC markers in control and azoxymethane and dextran sodium sulfate (AOM/DSS) groups at day 71 compared to that in the normal colonic mucosa. Arrows indicate the markers that are expressed at two-fold higher levels in the AOM/DSS group and two-fold lower levels in the DSS group compared to expression in the normal colonic mucosa. Red dotted lines indicate the threshold. ( E ) Comparison of relative mRNA expression of five markers in CAC. SEM, standard error of the mean. * P
    Figure Legend Snippet: Expression of tuft cell and progenitor cell markers in colitis-associated carcinogenesis (CAC). ( A ) Diagram of tuft cell and progenitor cell markers in the crypt. ( B and C ) Real-time PCR analysis of tuft cell marker Dclk1 and progenitor cell markers Prom1, Ephb2, and Msi1. Data represent the means ± SEM. (DSS: n = 4, AOM/DSS: n = 5). ( D ) Relative mRNA expression of ISC markers in control and azoxymethane and dextran sodium sulfate (AOM/DSS) groups at day 71 compared to that in the normal colonic mucosa. Arrows indicate the markers that are expressed at two-fold higher levels in the AOM/DSS group and two-fold lower levels in the DSS group compared to expression in the normal colonic mucosa. Red dotted lines indicate the threshold. ( E ) Comparison of relative mRNA expression of five markers in CAC. SEM, standard error of the mean. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Marker

    Expression of crypt base columnar (CBC) stem cell and +4 cell markers in colitis-associated carcinogenesis (CAC). ( A ) Schematic diagram of azoxymethane and dextran sodium sulfate (AOM/DSS)-induced colitis-associated colon cancer model. At the days indicated by arrows, mice (DSS: n = 4, AOM/DSS: n = 5) were sacrificed for analysis. ( B ) Body weight changes. Body weight at day 0: 100%. Data represent the mean ± SEM (DSS: n = 28, AOM/DSS: n = 35 at day 0). ( C ) Number of tumors ( > 1 mm in size) grossly detected in the colon. ( D ) Representative photos of colons harvested at day 58, 65, and 71. Arrows indicate visible tumors. ( E ) Diagram of CBC stem cells and +4 stem cells in the crypt, and their molecular markers. ( F and G ) Real-time PCR analysis for CBC stem cell markers; Lgr5, Ascl2, and Smoc2 and +4 stem cell markers; Bmi1, Hopx, Lrig1, and Tert in CAC. Data represent the means ± SEM. (DSS: n = 4, AOM/DSS: n = 5). SC, stem cell; ns, not significant, SEM: standard error of the mean. * P
    Figure Legend Snippet: Expression of crypt base columnar (CBC) stem cell and +4 cell markers in colitis-associated carcinogenesis (CAC). ( A ) Schematic diagram of azoxymethane and dextran sodium sulfate (AOM/DSS)-induced colitis-associated colon cancer model. At the days indicated by arrows, mice (DSS: n = 4, AOM/DSS: n = 5) were sacrificed for analysis. ( B ) Body weight changes. Body weight at day 0: 100%. Data represent the mean ± SEM (DSS: n = 28, AOM/DSS: n = 35 at day 0). ( C ) Number of tumors ( > 1 mm in size) grossly detected in the colon. ( D ) Representative photos of colons harvested at day 58, 65, and 71. Arrows indicate visible tumors. ( E ) Diagram of CBC stem cells and +4 stem cells in the crypt, and their molecular markers. ( F and G ) Real-time PCR analysis for CBC stem cell markers; Lgr5, Ascl2, and Smoc2 and +4 stem cell markers; Bmi1, Hopx, Lrig1, and Tert in CAC. Data represent the means ± SEM. (DSS: n = 4, AOM/DSS: n = 5). SC, stem cell; ns, not significant, SEM: standard error of the mean. * P

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction

    Enhanced Wnt signaling pathway in colitis-associated carcinogenesis. ( A ) Immunohistochemical analysis revealed that nuclear β-catenin staining was negative in all regenerative glands and low grade dysplasia (LGD) samples, but was positive in 37% of high grade dysplasia cases and 82% of adenocarcinomas (ADC). ( B ) Representative pictures of a LGD samples with membranous β-catenin and an ADC with strong cytoplasmic and nuclear β-catenin staining. Scale bar: 25 μm ( C ) Other Wnt-target genes including Axin2, Ephb3, Znrf3, and Rnf43 were upregulated in the azoxymethane and dextran sodium sulfate (AOM/DSS) group compared to expression in the normal and control groups. (Normal: n = 3, DSS: n = 7, AOM/DSS: n = 5). * P
    Figure Legend Snippet: Enhanced Wnt signaling pathway in colitis-associated carcinogenesis. ( A ) Immunohistochemical analysis revealed that nuclear β-catenin staining was negative in all regenerative glands and low grade dysplasia (LGD) samples, but was positive in 37% of high grade dysplasia cases and 82% of adenocarcinomas (ADC). ( B ) Representative pictures of a LGD samples with membranous β-catenin and an ADC with strong cytoplasmic and nuclear β-catenin staining. Scale bar: 25 μm ( C ) Other Wnt-target genes including Axin2, Ephb3, Znrf3, and Rnf43 were upregulated in the azoxymethane and dextran sodium sulfate (AOM/DSS) group compared to expression in the normal and control groups. (Normal: n = 3, DSS: n = 7, AOM/DSS: n = 5). * P

    Techniques Used: Immunohistochemistry, Staining, Expressing

    37) Product Images from "Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation"

    Article Title: Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation

    Journal: Mediators of Inflammation

    doi: 10.1155/2016/9453745

    Deletion of TRAF5 increases the protein expressions of the cytokines IFN- γ , IL-4, and IL-17a in the colons of mice induced by DSS. (a) The production of IFN- γ , IL-4, and IL-17a in the colons of DSS-induced mice or control mice was examined by ELISA ( N = 6 per group). (b) Representative immunofluorescence staining for IFN- γ , IL-4, and IL-17a in the colons of TRAF5 KO and WT mice (magnification 400x). (c) Quantification of positive cells ( N = 4 per group). The data are representative of 3 independent experiments (mean ± SD). ∗ p
    Figure Legend Snippet: Deletion of TRAF5 increases the protein expressions of the cytokines IFN- γ , IL-4, and IL-17a in the colons of mice induced by DSS. (a) The production of IFN- γ , IL-4, and IL-17a in the colons of DSS-induced mice or control mice was examined by ELISA ( N = 6 per group). (b) Representative immunofluorescence staining for IFN- γ , IL-4, and IL-17a in the colons of TRAF5 KO and WT mice (magnification 400x). (c) Quantification of positive cells ( N = 4 per group). The data are representative of 3 independent experiments (mean ± SD). ∗ p

    Techniques Used: Mouse Assay, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining

    Increased proportions of Th2 and IFN- γ /IL-17a-coproducing CD4 + T cells in the colons of TRAF5-deficient animals induced by DSS. LPMCs obtained from the colons of DSS-fed KO and WT mice were stimulated with PMA/ionomycin and subjected to surface staining for CD4. After fixation and permeabilization, intracellular staining for IL-4, IFN- γ , and IL-17a was performed as described in Section 2 . CD4 + T cells were then gated and analyzed. (a) Representative flow plots. The percentages of (b) Th2 cells (CD4 + IL-4 + ), (c) IFN- γ /IL-17a-coproducing CD4 + T cells (CD4 + IFN- γ + IL-17a + ), (d) classical Th1 cells (CD4 + IFN- γ + IL-17a − ), and (e) classical Th17 cells (CD4 + IL-17a + IFN- γ − ) are presented as the mean ± SD. The data are representative of 3 independent experiments. N = 6 per group. ∗∗ p
    Figure Legend Snippet: Increased proportions of Th2 and IFN- γ /IL-17a-coproducing CD4 + T cells in the colons of TRAF5-deficient animals induced by DSS. LPMCs obtained from the colons of DSS-fed KO and WT mice were stimulated with PMA/ionomycin and subjected to surface staining for CD4. After fixation and permeabilization, intracellular staining for IL-4, IFN- γ , and IL-17a was performed as described in Section 2 . CD4 + T cells were then gated and analyzed. (a) Representative flow plots. The percentages of (b) Th2 cells (CD4 + IL-4 + ), (c) IFN- γ /IL-17a-coproducing CD4 + T cells (CD4 + IFN- γ + IL-17a + ), (d) classical Th1 cells (CD4 + IFN- γ + IL-17a − ), and (e) classical Th17 cells (CD4 + IL-17a + IFN- γ − ) are presented as the mean ± SD. The data are representative of 3 independent experiments. N = 6 per group. ∗∗ p

    Techniques Used: Mouse Assay, Staining, Flow Cytometry

    Effect of TRAF5 deficiency on the histopathology and MPO activities of colon tissues. Histological evaluation of DSS-induced colitis was performed by microscopy and H E staining. Colon sections from TRAF5 KO and WT mice were scored in a blinded fashion, as described in Section 2 . (a) Representative cross sections of the distal colon. The magnifications of the images are 100-fold and 400-fold. (b) Quantitative results of the histological analysis ( N = 10 per group). (c) MPO activities in the colons were determined as described in Section 2 ( N = 6 per group). The data are presented as the mean ± SD. ∗ p
    Figure Legend Snippet: Effect of TRAF5 deficiency on the histopathology and MPO activities of colon tissues. Histological evaluation of DSS-induced colitis was performed by microscopy and H E staining. Colon sections from TRAF5 KO and WT mice were scored in a blinded fashion, as described in Section 2 . (a) Representative cross sections of the distal colon. The magnifications of the images are 100-fold and 400-fold. (b) Quantitative results of the histological analysis ( N = 10 per group). (c) MPO activities in the colons were determined as described in Section 2 ( N = 6 per group). The data are presented as the mean ± SD. ∗ p

    Techniques Used: Histopathology, Microscopy, Staining, Mouse Assay

    TRAF5 deficiency significantly enhances the activation of p65 in CD4 + T cells after the administration of DSS. (a) Representative immunofluorescence staining for p65. The p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (b) Quantification of p65 positive cells. (c) Representative immunofluorescence staining for CD4 and p65. The CD4-labeled cells show green fluorescence, p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (d) Quantification of p65 + CD4 + cells. (e) Representative immunofluorescence staining for CK18 and p65. The CK18-labeled cells show green fluorescence, p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (f) Quantification of p65 + CK18 + cells. The data are representative of 3 independent experiments (mean ± SD). N = 4 per group. ∗∗ p
    Figure Legend Snippet: TRAF5 deficiency significantly enhances the activation of p65 in CD4 + T cells after the administration of DSS. (a) Representative immunofluorescence staining for p65. The p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (b) Quantification of p65 positive cells. (c) Representative immunofluorescence staining for CD4 and p65. The CD4-labeled cells show green fluorescence, p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (d) Quantification of p65 + CD4 + cells. (e) Representative immunofluorescence staining for CK18 and p65. The CK18-labeled cells show green fluorescence, p65-labeled cells show red fluorescence, and the nuclei show blue fluorescence (magnification 400x). (f) Quantification of p65 + CK18 + cells. The data are representative of 3 independent experiments (mean ± SD). N = 4 per group. ∗∗ p

    Techniques Used: Activation Assay, Immunofluorescence, Staining, Labeling, Fluorescence

    TRAF5-deficient mice are more susceptible to DSS induction. (a) Change in percent body weight. (b) Change in DAI scores. ((c) and (d)) Mice were sacrificed on day 7, and their colons were removed, photographed, and measured in terms of length. The data are presented as the mean ± SD. N = 10 per group. ∗ p
    Figure Legend Snippet: TRAF5-deficient mice are more susceptible to DSS induction. (a) Change in percent body weight. (b) Change in DAI scores. ((c) and (d)) Mice were sacrificed on day 7, and their colons were removed, photographed, and measured in terms of length. The data are presented as the mean ± SD. N = 10 per group. ∗ p

    Techniques Used: Mouse Assay

    38) Product Images from "TLR2 Mediates Gap Junctional Intercellular Communication through Connexin-43 in Intestinal Epithelial Barrier Injury *"

    Article Title: TLR2 Mediates Gap Junctional Intercellular Communication through Connexin-43 in Intestinal Epithelial Barrier Injury *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M901619200

    GJ formation through Cx43 is altered in TLR2-deficient IEC in vivo . Cx43 is irregularly sequestered throughout the cytoplasm, and DSS-induced damage leads to complete loss of Cx43 in IEC, suggesting impairment of GJ pore formation in the absence of TLR2. Representative Cx43 (FITC, white )/propidium iodide ( blue ) immunofluorescence of the distal WT or TLR2-deficient colon with or without DSS exposure (4% for 5 days), as assessed by confocal laser microscopy (63×/1.4, oil, scan zoom 2.0). E marks IEC. The white arrowheads indicate representative regions of interest to show the loss of Cx43 in DSS-TLR2 −/− IEC. Insets show representative hematoxylin and eosin images (40×; gray-scaled ).
    Figure Legend Snippet: GJ formation through Cx43 is altered in TLR2-deficient IEC in vivo . Cx43 is irregularly sequestered throughout the cytoplasm, and DSS-induced damage leads to complete loss of Cx43 in IEC, suggesting impairment of GJ pore formation in the absence of TLR2. Representative Cx43 (FITC, white )/propidium iodide ( blue ) immunofluorescence of the distal WT or TLR2-deficient colon with or without DSS exposure (4% for 5 days), as assessed by confocal laser microscopy (63×/1.4, oil, scan zoom 2.0). E marks IEC. The white arrowheads indicate representative regions of interest to show the loss of Cx43 in DSS-TLR2 −/− IEC. Insets show representative hematoxylin and eosin images (40×; gray-scaled ).

    Techniques Used: In Vivo, Immunofluorescence, Microscopy

    TLR2-mediated IEC wound repair requires functional Cx43 in vivo . A , protocol scheme. WT (C57BL6/J) mice were exposed to DSS (2.3% in drinking water) for 5 days. Liposome-complexed siRNA targeting murine Cx43 or scrambled siRNA were administered per rectum once daily on days 3–5. After DSS exposure, the mice were treated with or without PCSK (days 5–7, 150 μg/ml; days 7–9, 50 μg/ml) and were sacrificed on day 9 ( n = 4–5/group). B , to evaluate knockdown of Cx43 in DSS-inflamed rectal EC, control mice ( n = 5/group) were sacrificed on day 5½. Compared with scrambled siRNA-treated DSS mice, expression of Cx43 protein (FITC, white , left panel , white arrowhead ) was only down-regulated in surface rectal epithelial cells of siCx43-treated DSS mice, but not in deeper crypt areas or underlying lamina propria cells ( black asterisk ), as assessed by multi-channel confocal immunofluorescence (63×/1.4, oil, scan zoom 2.0). The staining pattern of ZO-1 (CY5, white , right panel , blue arrowhead ) remained unchanged following siRNA treatment (nuclei were counterstained with DAPI ( blue )). The depth of surface rectal epithelial cells is marked by the white line. C and D , assessment of colon length ( C ) and histology ( D ) score with representative rectal cross-sections (hematoxylin and eosin; 10×) on day 9. The black asterisks indicate ulcers.
    Figure Legend Snippet: TLR2-mediated IEC wound repair requires functional Cx43 in vivo . A , protocol scheme. WT (C57BL6/J) mice were exposed to DSS (2.3% in drinking water) for 5 days. Liposome-complexed siRNA targeting murine Cx43 or scrambled siRNA were administered per rectum once daily on days 3–5. After DSS exposure, the mice were treated with or without PCSK (days 5–7, 150 μg/ml; days 7–9, 50 μg/ml) and were sacrificed on day 9 ( n = 4–5/group). B , to evaluate knockdown of Cx43 in DSS-inflamed rectal EC, control mice ( n = 5/group) were sacrificed on day 5½. Compared with scrambled siRNA-treated DSS mice, expression of Cx43 protein (FITC, white , left panel , white arrowhead ) was only down-regulated in surface rectal epithelial cells of siCx43-treated DSS mice, but not in deeper crypt areas or underlying lamina propria cells ( black asterisk ), as assessed by multi-channel confocal immunofluorescence (63×/1.4, oil, scan zoom 2.0). The staining pattern of ZO-1 (CY5, white , right panel , blue arrowhead ) remained unchanged following siRNA treatment (nuclei were counterstained with DAPI ( blue )). The depth of surface rectal epithelial cells is marked by the white line. C and D , assessment of colon length ( C ) and histology ( D ) score with representative rectal cross-sections (hematoxylin and eosin; 10×) on day 9. The black asterisks indicate ulcers.

    Techniques Used: Functional Assay, In Vivo, Mouse Assay, Expressing, Immunofluorescence, Staining

    39) Product Images from "Expression of inositol-requiring enzyme 1β is downregulated in azoxymethane/dextran sulfate sodium-induced mouse colonic tumors"

    Article Title: Expression of inositol-requiring enzyme 1β is downregulated in azoxymethane/dextran sulfate sodium-induced mouse colonic tumors

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2019.7317

    IRE1α and IRE1β protein expression is decreased in mice receiving AOM/DSS treatment. Following a one-off treatment with AOM and three cycles of DSS, tumor tissues from mice in the tumor group (n=10) and colon tissues from mice in the untreated control group (n=10) were collected. (A) IRE1α and (B) IRE1β protein expression was assessed by western blotting. The reduction of IRE1α expression was not significant, but the expression of IRE1β decreased significantly. *P
    Figure Legend Snippet: IRE1α and IRE1β protein expression is decreased in mice receiving AOM/DSS treatment. Following a one-off treatment with AOM and three cycles of DSS, tumor tissues from mice in the tumor group (n=10) and colon tissues from mice in the untreated control group (n=10) were collected. (A) IRE1α and (B) IRE1β protein expression was assessed by western blotting. The reduction of IRE1α expression was not significant, but the expression of IRE1β decreased significantly. *P

    Techniques Used: Expressing, Mouse Assay, Western Blot

    AOM/DSS treatment increases mRNA levels of inflammatory cytokines in mice. Following a one-off treatment with AOM and three cycles of DSS, IL-6, IL-8 and TNF-α mRNA expression levels were determined in mice of the tumor and the untreated control group (n=10/group) using reverse transcription-quantitative polymerase chain reaction assays. *P
    Figure Legend Snippet: AOM/DSS treatment increases mRNA levels of inflammatory cytokines in mice. Following a one-off treatment with AOM and three cycles of DSS, IL-6, IL-8 and TNF-α mRNA expression levels were determined in mice of the tumor and the untreated control group (n=10/group) using reverse transcription-quantitative polymerase chain reaction assays. *P

    Techniques Used: Mouse Assay, Expressing, Real-time Polymerase Chain Reaction

    40) Product Images from "Comparisons of gut microbiota profiles in wild-type and gelatinase B/matrix metalloproteinase-9-deficient mice in acute DSS-induced colitis"

    Article Title: Comparisons of gut microbiota profiles in wild-type and gelatinase B/matrix metalloproteinase-9-deficient mice in acute DSS-induced colitis

    Journal: NPJ Biofilms and Microbiomes

    doi: 10.1038/s41522-018-0059-0

    Differences in microbiota composition at genus level between control and DSS-treated mice with LEfSe (Linear discriminant analysis Effect Size). Genera indicated in blue were more abundantly present in control mice, whereas genera in red were found to be more abundant in mice with DSS-induced colitis. No differences were observed when subdividing according to genotype (WT or MMP-9 -/- ). LDA linear discriminant analysis
    Figure Legend Snippet: Differences in microbiota composition at genus level between control and DSS-treated mice with LEfSe (Linear discriminant analysis Effect Size). Genera indicated in blue were more abundantly present in control mice, whereas genera in red were found to be more abundant in mice with DSS-induced colitis. No differences were observed when subdividing according to genotype (WT or MMP-9 -/- ). LDA linear discriminant analysis

    Techniques Used: Mouse Assay

    Drivers of changes in fecal microbiota composition at the genus level. Bar plot depicting the relative abundance of the 10 most abundant genera in all samples. Samples are divided per cage (A, B, C, D, F, G, I, J, K, L, N, and Q) and the four respective phenotype–genotype combinations (DSS.MMP-9 -/- , DSS.WT, control.MMP-9 -/- , and control.WT). The color intensities of the bars represent the disease activity index (DAI) with brighter colors indicating higher inflammatory burden. Each bar of the histogram represents the cumulative relative abundance of all samples within one group and the line within each bar indicates the separation of each sample within the group. If no line is observed within the bar, only one sample was available
    Figure Legend Snippet: Drivers of changes in fecal microbiota composition at the genus level. Bar plot depicting the relative abundance of the 10 most abundant genera in all samples. Samples are divided per cage (A, B, C, D, F, G, I, J, K, L, N, and Q) and the four respective phenotype–genotype combinations (DSS.MMP-9 -/- , DSS.WT, control.MMP-9 -/- , and control.WT). The color intensities of the bars represent the disease activity index (DAI) with brighter colors indicating higher inflammatory burden. Each bar of the histogram represents the cumulative relative abundance of all samples within one group and the line within each bar indicates the separation of each sample within the group. If no line is observed within the bar, only one sample was available

    Techniques Used: Activity Assay

    Clinical and macroscopic parameters of DSS-induced inflammation in WT and MMP-9 -/- mice. a Representation of the acute DSS model. DSS-exposed mice comprised of WT mice ( n = 10) and MMP-9 -/- mice ( n = 10). Control mice received normal drinking water throughout the experiment (WT mice ( n = 10), MMP-9 -/- mice ( n = 10)). All groups consisted of five males and five females. b Relative weight loss from the start of the experiment until the time of sacrifice (* day 9). c Absolute weight loss at the time of sacrifice. d Disease activity index including stools, blood, and weight loss at the time of sacrifice. e Colon weight/length (w/l) ratio. f Macroscopic damage score including mesenterial colonic adhesion, hyperemia along the colon, and length of colonic inflammation. Medians with interquartile ranges are shown and Mann–Whitney U tests were performed (*** p
    Figure Legend Snippet: Clinical and macroscopic parameters of DSS-induced inflammation in WT and MMP-9 -/- mice. a Representation of the acute DSS model. DSS-exposed mice comprised of WT mice ( n = 10) and MMP-9 -/- mice ( n = 10). Control mice received normal drinking water throughout the experiment (WT mice ( n = 10), MMP-9 -/- mice ( n = 10)). All groups consisted of five males and five females. b Relative weight loss from the start of the experiment until the time of sacrifice (* day 9). c Absolute weight loss at the time of sacrifice. d Disease activity index including stools, blood, and weight loss at the time of sacrifice. e Colon weight/length (w/l) ratio. f Macroscopic damage score including mesenterial colonic adhesion, hyperemia along the colon, and length of colonic inflammation. Medians with interquartile ranges are shown and Mann–Whitney U tests were performed (*** p

    Techniques Used: Mouse Assay, Activity Assay, MANN-WHITNEY

    Fecal microbiota diversity in control and DSS-treated MMP-9 -/- mice and WT littermates. a Box plot representation of microbiota richness (number of observed operational taxonomic units [OTUs] per sample) distribution across MMP-9 -/- and WT mice. b Variation in microbial community composition represented by a principal coordinates analysis (PCoA) of the Bray–Curtis dissimilarity matrix, calculated from the OTU-level relative abundance matrix. Pheno.geno indicates the combination of phenotype (control or DSS) and genotype (WT or MMP-9 -/- ) within each of the four experimental groups
    Figure Legend Snippet: Fecal microbiota diversity in control and DSS-treated MMP-9 -/- mice and WT littermates. a Box plot representation of microbiota richness (number of observed operational taxonomic units [OTUs] per sample) distribution across MMP-9 -/- and WT mice. b Variation in microbial community composition represented by a principal coordinates analysis (PCoA) of the Bray–Curtis dissimilarity matrix, calculated from the OTU-level relative abundance matrix. Pheno.geno indicates the combination of phenotype (control or DSS) and genotype (WT or MMP-9 -/- ) within each of the four experimental groups

    Techniques Used: Mouse Assay

    Fecal microbiota profiles in control and DSS-treated MMP-9 -/- mice and WT littermates. Relative abundances at phylum level a and at genus level b are shown for the four experimental groups (DSS.MMP-9 -/- , DSS.WT, control.MMP-9 -/- , and control.WT). The top 20 most abundant genera are represented
    Figure Legend Snippet: Fecal microbiota profiles in control and DSS-treated MMP-9 -/- mice and WT littermates. Relative abundances at phylum level a and at genus level b are shown for the four experimental groups (DSS.MMP-9 -/- , DSS.WT, control.MMP-9 -/- , and control.WT). The top 20 most abundant genera are represented

    Techniques Used: Mouse Assay

    Analysis of the microbiota composition with genotype as constrained variable. Differences in microbiota composition between WT and MMP-9 -/- mice within the control a and DSS b phenotype. The plots show the distance-based redundancy analysis performed with capscale function (vegan package). Dots represent individual samples plotted according to their specific CAP1 and MDS1 coordinates and the dotted lines connect the samples with their corresponding genotype (MMP-9 -/- in blue and WT in red). Genera with a |CAP| > 0.1 are indicated on the plot and the arrow represents the CAP1 and MDS1 coordinates of each genus. CAP canonical analysis of principal coordinates, MDS multidimensional scaling
    Figure Legend Snippet: Analysis of the microbiota composition with genotype as constrained variable. Differences in microbiota composition between WT and MMP-9 -/- mice within the control a and DSS b phenotype. The plots show the distance-based redundancy analysis performed with capscale function (vegan package). Dots represent individual samples plotted according to their specific CAP1 and MDS1 coordinates and the dotted lines connect the samples with their corresponding genotype (MMP-9 -/- in blue and WT in red). Genera with a |CAP| > 0.1 are indicated on the plot and the arrow represents the CAP1 and MDS1 coordinates of each genus. CAP canonical analysis of principal coordinates, MDS multidimensional scaling

    Techniques Used: Mouse Assay

    Related Articles

    Mouse Assay:

    Article Title: Cow and Human Milk-Derived Exosomes Ameliorate Colitis in DSS Murine Model
    Article Snippet: .. Dextran Sulfate Sodium-Induced Colitis Model in MiceColitis was induced in 8-weeks male Balb/c mice (Envigo RMS, Israel) using 5% DSS (dextran sulfate sodium salt, colitis grade (36,000–50,000) (MP Biomedicals, LLC, France) provided for 7 days in the drinking water. ..

    Article Title: Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice
    Article Snippet: .. CAC was induced in 8 weeks old female C57BL/6 mice by a single intraperitoneal injection of azoxymethane (AOM, 12 mg/kg) (Sigma-Aldrich) and subsequent oral administration of 2 % dextran sulfate sodium salt (DSS) (MW 36,000-50,0000Da, MP Biomedicals) in drinking water ad libitum for 5 consecutive days in 3 intermittent cycles of DSS interrupted by 2-week periods without DSS challenge. .. Mice were sacrificed 8 weeks after the first day of the first DSS cycle.

    Article Title: Diet High in Soybean Oil Increases Susceptibility to Colitis in Mice
    Article Snippet: At the end of the study, mice were euthanized by carbon dioxide inhalation, in accordance with NIH guidelines. .. Dextran sulfate sodium (DSS) treatment WT or α1HMZ mice that had been on the diets for 8 to 15 weeks were treated with 2.5% dextran sodium sulfate salt (DSS) (reagent grade, MW 3.6–5 kDa, MP Biomedicals, #160110, Santa Ana, CA) in water ad libitum for six days and sacrificed immediately or allowed to recover up to 3 days with tap water. .. Mice were continued on the same diet before, during and after DSS treatment and monitored daily for changes in body weight, stool consistency, ruffled fur and activity level.

    Article Title: Thrombospondin-1 Type 1 Repeats in a Model of Inflammatory Bowel Disease: Transcript Profile and Therapeutic Effects
    Article Snippet: .. Dextran sulfate sodium (DSS) and TSR Treatments DSS (MW: 36,000∼50,000) (MP Biomedical, LLC, Aurora, OH) was dissolved in the drinking water (distilled) of the mice at a dilution of 2.5% (wt/vol) and administered to 6–7 week old mice for 7 days to induce acute colitis. .. Simultaneously, mice were subcutaneously injected daily with the following recombinant proteins: 3TSR (n = 10), TSR2 (n = 9) TSR2+RFK (n = 15).

    Article Title: Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges
    Article Snippet: After euthanasia, colitis severity was assessed by measuring spleen and colon weight as well as colonic myeloperoxidase (MPO) activity and cytokine production. .. Dextran Sulfate Sodium (DSS) treatment Six to eight week-old WT and N4KO male mice (≈22 g) received 2% (w/v) DSS (MW = 36,000–50,000 kDa, MP Biomedicals, Solon, OH) in drinking water for 6 days to induce colon injury. ..

    Article Title: Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity
    Article Snippet: .. Opg −/− mice and co-housed WT mice or littermate Opg +/− mice consumed DSS (dextran sulfate sodium salt; MP Biomedicals LLC., Santa Ana, CA, USA) in their drinking water for up to 8 days. .. On the basis of the results of preliminary experiments undertaken in each facility to estimate the optimal DSS concentration, we set the DSS concentration at 2.5% for Hokkaido University and at 1.5% for IMSUT.

    Injection:

    Article Title: Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice
    Article Snippet: .. CAC was induced in 8 weeks old female C57BL/6 mice by a single intraperitoneal injection of azoxymethane (AOM, 12 mg/kg) (Sigma-Aldrich) and subsequent oral administration of 2 % dextran sulfate sodium salt (DSS) (MW 36,000-50,0000Da, MP Biomedicals) in drinking water ad libitum for 5 consecutive days in 3 intermittent cycles of DSS interrupted by 2-week periods without DSS challenge. .. Mice were sacrificed 8 weeks after the first day of the first DSS cycle.

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    Depletion of macrophages reduces the severity of <t>DSS-induced</t> colitis promoted by <t>NaCl.</t> A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P
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    EPO Treatment Downregulates Proinflammatory Immune Pathways and Improves Disease Activity in <t>DSS-Induced</t> Colitis Epor −/− mice and Epor +/+ littermates on a <t>C57BL/6</t> background were administered 3% DSS dissolved in water or water alone (controls) for 7 consecutive days. Thereafter, DSS was replaced by drinking water and all animals were followed up for another 7 days. Subsequently, mice were injected with EPO (or PBS) on days 7, 8, and 9 after induction of colitis as indicated by arrows. (A) Changes in body weight as combined from two independent experiments and 5–14 DSS-treated mice per group are presented and were compared as detailed in the legend to Figure 6 . Data of mice receiving drinking water are not depicted. Statistical significant differences between DSS-treated Epor +/+ mice receiving either PBS or EPO are indicated. (B) Histopathological colitis scores for mice administered either water or DSS (n = 5–14 per group) with each point representing an individual mouse. (C and D) qRT-PCR analysis of immune response genes (C) and NF-κB p65 binding activity (D) in colons of these mice (n = 5–14 per group).
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    Valiant aom dss induced colitis
    Restoring miR-148a expression attenuates spontaneous and <t>AOM/dextran</t> sodium sulfate <t>(DSS)-induced</t> tumorigenesis. ( a ) Body weight changes of WT and miR-148a KO mice treated with lentivirus containing Pri-miR-148a or control expression vector during AOM/DSS treatment ( n =9–12). ( b ) Typical images of colon tumors of mice from ( a ) 120 days after AOM/DSS treatment. ( c and d ) Colon tumor number ( c , Left), averge volume ( c , right) and size ( d ) in mice from panel ( b ). ( e ) Inhibition of NF- κ B and STAT3 signaling was determined in the colons collected in mice from panel ( b ). Each lane represents an individual mouse. ( f ) Cytokine levels were determined by ELISA in colon tissues collected in mice from panel ( b ). ( g and h ) Colon tumor number ( g , Top), average volume ( g , Bottom) and size ( h ) in Apc min/+ mice treated with lentivirus containing Pri-miR-148a or a control expression vector. ( i ) Small intestine tumor number (Top) and average volume (Bottom) in Apc min/+ mice from panel ( g ) ( n =9–10). Data present mean±S.D. in panels ( a, d and h ). * P
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    Image Search Results


    Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: Depletion of macrophages reduces the severity of DSS-induced colitis promoted by NaCl. A: Clodronate liposomes (denoted as MDP) or control PBS-liposomes (denoted as PBS) were administrated intravenously to all mice, as the schematic protocol indicated during DSS and NaCl treatment; B: The disease activity index was monitored daily; C: Colon length was measured in each group of mice ( n = 10); D: Colon explants were cultured for 24 h and the inflammatory cytokines in supernatants were detected by enzyme-linked immunosorbent assay ( n = 3). a P

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Activity Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

    NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: NaCl promotes CD4 + IFN-γ + IL-17 + T cell increase and inflammatory cytokine secretion in DSS-treated mice. A: The CD4 + IFN-γ + IL-17 + T cells in LP, MLN and SP from mice treated with NaCl and/or DSS were detected by flow cytometry; B: Combined flow cytometry data of CD4 + IL-17 + , CD4 + IFN-γ + and CD4 + IFN-γ + IL-17 + T cell subsets distribution in LP, MLN and SP; C: Colon tissues collected from mice treated with DSS or DSS + NaCl, which were washed with phosphate-buffered saline and cultured for 24 h, and the supernatants were collected and detected by enzyme-linked immunosorbent assay; D: Colon tissues collected from mice treated with NaCl and DSS (or only DSS) were detected by RT-PCR. The relative fold-change in DSS + NaCl-treated mice vs DSS-treated mice. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Flow Cytometry, Cytometry, Cell Culture, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: CD11b + macrophages are increased in DSS- and NaCl-treated mice. A: The CD11b + cells in LP, MLN and SP from the four groups were detected by flow cytometry; B: Quantification of the flow cytometry data indicates the CD11b + cell distribution in LP, MLN and SP. In the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Flow Cytometry, Cytometry

    CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: CD3 + CD4 + CD25 + Foxp3 + T cells are increased in mice treated with DSS and NaCl. A: CD3 + CD4 + CD25 + Foxp3 + T cells in LP, MLN and SP from animal models were detected by flow cytometry; B: A summary of the percentages of CD3 + CD4 + CD25 + Foxp3 + T cell distribution in LP, MLN and SP; C: LPMCs from the four groups were isolated and cultured for 24 h, and the levels of cytokines in the culture supernatants were collected and analyzed by enzyme-linked immunosorbent assay. In all the panels, data indicate three separate experiments, whereby 3 mice per group were used in each experiment. a P

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Flow Cytometry, Cytometry, Isolation, Cell Culture, Enzyme-linked Immunosorbent Assay

    iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: iNOS + F4/80 + macrophages increase in the colon of DSS- and NaCl-treated mice. Macrophages in colon tissue obtained from mice injected intraperitoneally with PBS-containing liposomes (denoted as PBS), or clodronate liposomes (denoted as MDP) during the NaCl and DSS treatment were analyzed. The sections were stained with antibodies of anti-F4/80 (red) and anti-iNOS (green). Nuclei were stained with DAPI (blue). Laser confocal microscopy was used to detect fluorescence. (Scale bar = 50 μm). DSS: Dextran sulfate sodium; iNOS: inducible nitric oxide synthase.

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Injection, Staining, Confocal Microscopy, Fluorescence

    Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P

    Journal: World Journal of Gastroenterology

    Article Title: Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

    doi: 10.3748/wjg.v24.i16.1779

    Figure Lengend Snippet: Mice treated with DSS and NaCl develop more severe colitis. A: Mice were given DSS and/or NaCl, and were weighed daily; B: Death status was recorded daily; C: Colonic tissues were collected from four groups of mice and colonic length was measured; D: Histological analyses show sections of the colon stained with HE for DSS- or NaCl-treated mice. In all the panels, data indicate three separate experiments, whereby 10 mice per group were used in each experiment. a P

    Article Snippet: They received water containing 2% NaCl (Sinopharm Chemical Reagent, China) and/or water containing 2.5% DSS (160110; MP Biomedicals, United States) for 10 d. The intestinal macrophages were depleted using MDP (van Rooijen and van Kesteren-Hendrikx, 2003, clodronateliposomes.org, Holland)[ ].

    Techniques: Mouse Assay, Staining

    Commensal-specific antibody production is increased in Opg −/− mice. a , d Schematic cartoons depicting experimental designs. Commensal-specific fecal or serum immunoglobulins were detected by flow cytometry. b , c , e , f Feces and sera were collected from Opg −/− or co-housed WT mice at day 0 ( b , e ) or day 5 ( c , f ) after the onset of DSS consumption. Flow cytometry assays of DAPI-positive fecal bacteria bound by the indicated Igs were performed without ( b , c ) or with ( e , f ) serum. Representative data from two independent experiments are shown as the mean ± standard deviation. * p

    Journal: Nature Communications

    Article Title: Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity

    doi: 10.1038/s41467-019-13883-y

    Figure Lengend Snippet: Commensal-specific antibody production is increased in Opg −/− mice. a , d Schematic cartoons depicting experimental designs. Commensal-specific fecal or serum immunoglobulins were detected by flow cytometry. b , c , e , f Feces and sera were collected from Opg −/− or co-housed WT mice at day 0 ( b , e ) or day 5 ( c , f ) after the onset of DSS consumption. Flow cytometry assays of DAPI-positive fecal bacteria bound by the indicated Igs were performed without ( b , c ) or with ( e , f ) serum. Representative data from two independent experiments are shown as the mean ± standard deviation. * p

    Article Snippet: Opg −/− mice and co-housed WT mice or littermate Opg +/− mice consumed DSS (dextran sulfate sodium salt; MP Biomedicals LLC., Santa Ana, CA, USA) in their drinking water for up to 8 days.

    Techniques: Mouse Assay, Flow Cytometry, Cytometry, Standard Deviation

    Absence of Opg ameliorates DSS-induced colitis. a Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b Colon length was measured after sacrifice at day 8. c Representative histology of hematoxylin- and eosin-stained colonic tissue from WT and Opg −/− mice with DSS-induced colitis on day 8. d Stool scores were measured as described in the Methods. e Spleen weight was measured after sacrifice at day 8. a , b , d , and e Data are presented as the mean ± SEM. ** p

    Journal: Nature Communications

    Article Title: Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity

    doi: 10.1038/s41467-019-13883-y

    Figure Lengend Snippet: Absence of Opg ameliorates DSS-induced colitis. a Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b Colon length was measured after sacrifice at day 8. c Representative histology of hematoxylin- and eosin-stained colonic tissue from WT and Opg −/− mice with DSS-induced colitis on day 8. d Stool scores were measured as described in the Methods. e Spleen weight was measured after sacrifice at day 8. a , b , d , and e Data are presented as the mean ± SEM. ** p

    Article Snippet: Opg −/− mice and co-housed WT mice or littermate Opg +/− mice consumed DSS (dextran sulfate sodium salt; MP Biomedicals LLC., Santa Ana, CA, USA) in their drinking water for up to 8 days.

    Techniques: Staining, Mouse Assay

    Non-hematopoietic cells in Opg −/− mice contribute to relief of DSS colitis symptoms. a , e Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b , f Fecal clinical scores were measured as described in the Methods. c , g Colon length was measured after sacrifice at day 8. d , h Spleen weight was measured after sacrifice at day 8. WT or Opg −/− recipient mice following bone marrow transplantation from WT donors ( a – d ) and WT recipient mice following bone marrow transplantation from WT or Opg −/− donors ( e – h ) treated with 1.5% DSS for 7 days. Data are representative of two independent experiments. ** p

    Journal: Nature Communications

    Article Title: Osteoprotegerin-dependent M cell self-regulation balances gut infection and immunity

    doi: 10.1038/s41467-019-13883-y

    Figure Lengend Snippet: Non-hematopoietic cells in Opg −/− mice contribute to relief of DSS colitis symptoms. a , e Daily changes in body weight during dextran sodium sulfate (DSS)-induced colitis. Changes in body weight percentage were calculated by dividing the body weight on the specified day by the body weight at day 0. b , f Fecal clinical scores were measured as described in the Methods. c , g Colon length was measured after sacrifice at day 8. d , h Spleen weight was measured after sacrifice at day 8. WT or Opg −/− recipient mice following bone marrow transplantation from WT donors ( a – d ) and WT recipient mice following bone marrow transplantation from WT or Opg −/− donors ( e – h ) treated with 1.5% DSS for 7 days. Data are representative of two independent experiments. ** p

    Article Snippet: Opg −/− mice and co-housed WT mice or littermate Opg +/− mice consumed DSS (dextran sulfate sodium salt; MP Biomedicals LLC., Santa Ana, CA, USA) in their drinking water for up to 8 days.

    Techniques: Mouse Assay, Transplantation Assay

    EPO Treatment Downregulates Proinflammatory Immune Pathways and Improves Disease Activity in DSS-Induced Colitis Epor −/− mice and Epor +/+ littermates on a C57BL/6 background were administered 3% DSS dissolved in water or water alone (controls) for 7 consecutive days. Thereafter, DSS was replaced by drinking water and all animals were followed up for another 7 days. Subsequently, mice were injected with EPO (or PBS) on days 7, 8, and 9 after induction of colitis as indicated by arrows. (A) Changes in body weight as combined from two independent experiments and 5–14 DSS-treated mice per group are presented and were compared as detailed in the legend to Figure 6 . Data of mice receiving drinking water are not depicted. Statistical significant differences between DSS-treated Epor +/+ mice receiving either PBS or EPO are indicated. (B) Histopathological colitis scores for mice administered either water or DSS (n = 5–14 per group) with each point representing an individual mouse. (C and D) qRT-PCR analysis of immune response genes (C) and NF-κB p65 binding activity (D) in colons of these mice (n = 5–14 per group).

    Journal: Immunity

    Article Title: Erythropoietin Contrastingly Affects Bacterial Infection and Experimental Colitis by Inhibiting Nuclear Factor-?B-Inducible Immune Pathways

    doi: 10.1016/j.immuni.2011.01.002

    Figure Lengend Snippet: EPO Treatment Downregulates Proinflammatory Immune Pathways and Improves Disease Activity in DSS-Induced Colitis Epor −/− mice and Epor +/+ littermates on a C57BL/6 background were administered 3% DSS dissolved in water or water alone (controls) for 7 consecutive days. Thereafter, DSS was replaced by drinking water and all animals were followed up for another 7 days. Subsequently, mice were injected with EPO (or PBS) on days 7, 8, and 9 after induction of colitis as indicated by arrows. (A) Changes in body weight as combined from two independent experiments and 5–14 DSS-treated mice per group are presented and were compared as detailed in the legend to Figure 6 . Data of mice receiving drinking water are not depicted. Statistical significant differences between DSS-treated Epor +/+ mice receiving either PBS or EPO are indicated. (B) Histopathological colitis scores for mice administered either water or DSS (n = 5–14 per group) with each point representing an individual mouse. (C and D) qRT-PCR analysis of immune response genes (C) and NF-κB p65 binding activity (D) in colons of these mice (n = 5–14 per group).

    Article Snippet: Establishment of DSS-Colitis DSS-colitis was induced in male C57BL/6 Epor+/+ and Epor−/− age-matched littermates (10–14 weeks) with 3% dextran sulfate sodium (DSS; from MP Biomedicals) in accordance with an established protocol with modifications as described in .

    Techniques: Activity Assay, Mouse Assay, Injection, Quantitative RT-PCR, Binding Assay

    Restoring miR-148a expression attenuates spontaneous and AOM/dextran sodium sulfate (DSS)-induced tumorigenesis. ( a ) Body weight changes of WT and miR-148a KO mice treated with lentivirus containing Pri-miR-148a or control expression vector during AOM/DSS treatment ( n =9–12). ( b ) Typical images of colon tumors of mice from ( a ) 120 days after AOM/DSS treatment. ( c and d ) Colon tumor number ( c , Left), averge volume ( c , right) and size ( d ) in mice from panel ( b ). ( e ) Inhibition of NF- κ B and STAT3 signaling was determined in the colons collected in mice from panel ( b ). Each lane represents an individual mouse. ( f ) Cytokine levels were determined by ELISA in colon tissues collected in mice from panel ( b ). ( g and h ) Colon tumor number ( g , Top), average volume ( g , Bottom) and size ( h ) in Apc min/+ mice treated with lentivirus containing Pri-miR-148a or a control expression vector. ( i ) Small intestine tumor number (Top) and average volume (Bottom) in Apc min/+ mice from panel ( g ) ( n =9–10). Data present mean±S.D. in panels ( a, d and h ). * P

    Journal: Cell Death and Differentiation

    Article Title: miR-148a inhibits colitis and colitis-associated tumorigenesis in mice

    doi: 10.1038/cdd.2017.151

    Figure Lengend Snippet: Restoring miR-148a expression attenuates spontaneous and AOM/dextran sodium sulfate (DSS)-induced tumorigenesis. ( a ) Body weight changes of WT and miR-148a KO mice treated with lentivirus containing Pri-miR-148a or control expression vector during AOM/DSS treatment ( n =9–12). ( b ) Typical images of colon tumors of mice from ( a ) 120 days after AOM/DSS treatment. ( c and d ) Colon tumor number ( c , Left), averge volume ( c , right) and size ( d ) in mice from panel ( b ). ( e ) Inhibition of NF- κ B and STAT3 signaling was determined in the colons collected in mice from panel ( b ). Each lane represents an individual mouse. ( f ) Cytokine levels were determined by ELISA in colon tissues collected in mice from panel ( b ). ( g and h ) Colon tumor number ( g , Top), average volume ( g , Bottom) and size ( h ) in Apc min/+ mice treated with lentivirus containing Pri-miR-148a or a control expression vector. ( i ) Small intestine tumor number (Top) and average volume (Bottom) in Apc min/+ mice from panel ( g ) ( n =9–10). Data present mean±S.D. in panels ( a, d and h ). * P

    Article Snippet: The DSS and AOM/DSS-induced colitis and CAC mouse models followed previously described protocols., Briefly, for colitis, WT or miR-148a KO mice were provided with 3.5% DSS (216011080, MW=36-50KD; MP Biomedicals, Santa Ana, CA, USA) in drinking water for 6 days, followed by regular drinking water.

    Techniques: Expressing, Mouse Assay, Plasmid Preparation, Inhibition, Enzyme-linked Immunosorbent Assay

    miR-148a KO mice are more susceptible to AOM/dextran sodium sulfate (DSS)-induced colorectal tumorigenesis. ( a ) Changes of miR-148a-3p/5p expression in colon tissues collected from WT mice at days 0, 30 and 120 after AOM/DSS treatment. ( a – j ) WT and miR-148a KO mice were injected with AOM on day 0 and were treated with three rounds of DSS for 7 days. ( b ) Body weight changes of WT ( n =26) and miR-148a KO ( n =37) mice. ( c ) Survival analysis. ( d ) Typical images of colon tumors from WT and miR-148a KO mice 120 days after AOM/DSS treatment. ( e ) Colon length (Top) and weight (Bottom) were determined from WT ( n =13) and miR-148a KO ( n =16) mice on day 120 after AOM/DSS treatment. ( f and g ) Colon tumor number ( f , Left), average volume ( f , right) and size ( g ) in WT ( n =13) and miR-148a KO ( n =16) mice from panel ( d ). ( h ) Colon tissues collected from panel ( d ) were fixed, stained with hematoxylin and eosin (H E; Top) and immuno-stained for Ki-67 (Bottom). Scale bars, 100 μ m. ( i ) Activation of NF- κ B and STAT3 signaling were determined in the colons collected from WT and miR-148a KO mice from panel ( d ). Each lane represents an individual mouse. ( j ) The levels of the indicated cytokines were determined by ELISA in colon tissues collected from WT and miR-148a KO mice from panel ( d ). Data present mean±S.D. in panels ( a , b and g ). * P

    Journal: Cell Death and Differentiation

    Article Title: miR-148a inhibits colitis and colitis-associated tumorigenesis in mice

    doi: 10.1038/cdd.2017.151

    Figure Lengend Snippet: miR-148a KO mice are more susceptible to AOM/dextran sodium sulfate (DSS)-induced colorectal tumorigenesis. ( a ) Changes of miR-148a-3p/5p expression in colon tissues collected from WT mice at days 0, 30 and 120 after AOM/DSS treatment. ( a – j ) WT and miR-148a KO mice were injected with AOM on day 0 and were treated with three rounds of DSS for 7 days. ( b ) Body weight changes of WT ( n =26) and miR-148a KO ( n =37) mice. ( c ) Survival analysis. ( d ) Typical images of colon tumors from WT and miR-148a KO mice 120 days after AOM/DSS treatment. ( e ) Colon length (Top) and weight (Bottom) were determined from WT ( n =13) and miR-148a KO ( n =16) mice on day 120 after AOM/DSS treatment. ( f and g ) Colon tumor number ( f , Left), average volume ( f , right) and size ( g ) in WT ( n =13) and miR-148a KO ( n =16) mice from panel ( d ). ( h ) Colon tissues collected from panel ( d ) were fixed, stained with hematoxylin and eosin (H E; Top) and immuno-stained for Ki-67 (Bottom). Scale bars, 100 μ m. ( i ) Activation of NF- κ B and STAT3 signaling were determined in the colons collected from WT and miR-148a KO mice from panel ( d ). Each lane represents an individual mouse. ( j ) The levels of the indicated cytokines were determined by ELISA in colon tissues collected from WT and miR-148a KO mice from panel ( d ). Data present mean±S.D. in panels ( a , b and g ). * P

    Article Snippet: The DSS and AOM/DSS-induced colitis and CAC mouse models followed previously described protocols., Briefly, for colitis, WT or miR-148a KO mice were provided with 3.5% DSS (216011080, MW=36-50KD; MP Biomedicals, Santa Ana, CA, USA) in drinking water for 6 days, followed by regular drinking water.

    Techniques: Mouse Assay, Expressing, Injection, Staining, Activation Assay, Enzyme-linked Immunosorbent Assay

    miR-148a expression in both bone marrow and non-bone marrow contributes to attenuation of colitis and colorectal tumorigenesis. ( a ) Body weight changes of the indicated miR-148a bone marrow chimera mice after dextran sodium sulfate (DSS) treatment ( n =10–12). ( a – g ) miR-148a bone marrow chimera mice were treated with 3.5% DSS in drinking water for 6 days. ( b ) Rectal bleeding (Left) and stool consistency (Right) were scored daily. ( c ) Survival of the indicated miR-148a bone marrow chimera mice after DSS treatment. ( d ) Colon length from indicated miR-148a bone marrow chimera mice on day 9 after DSS treatment. ( e ) Activation of NF- κ B and STAT3 signaling in colon tissues was determined by immuno-blotting on day 9. Each lane represents an individual mouse. ( f ) mRNA (Top) and protein (Bottom) levels of the indicated cytokines were determined by reverse transcription quantitative-PCR and ELISA, respectively, in colon tissues on day 9. ( g ) Colon tissues on day 9 after DSS treatment were fixed, stained with hematoxylin and eosin (H E; Left) and immuno-stained for the macrophage marker F4/80 (Right). Scale bars, 100 μ m. ( h ) Typical images of colon tumors from the indicated miR-148a bone marrow chimera mice 120 days after AOM/DSS treatment. ( h – k ) miR-148a bone marrow chimera mice were injected with AOM on day 0 and treated with three rounds of 2.5% DSS in drinking water for 7 days. ( i and j ) Colon tumor number ( i , Left), averge tumor volume ( i , right) and size ( j ) in the indicated miR-148a bone marrow chimera mice 120 days after AOM/DSS treatment. ( k ) Colon weight from mice in panel ( i ). Data indicate the mean±S.D. in panels ( a , b , f and j ). * P

    Journal: Cell Death and Differentiation

    Article Title: miR-148a inhibits colitis and colitis-associated tumorigenesis in mice

    doi: 10.1038/cdd.2017.151

    Figure Lengend Snippet: miR-148a expression in both bone marrow and non-bone marrow contributes to attenuation of colitis and colorectal tumorigenesis. ( a ) Body weight changes of the indicated miR-148a bone marrow chimera mice after dextran sodium sulfate (DSS) treatment ( n =10–12). ( a – g ) miR-148a bone marrow chimera mice were treated with 3.5% DSS in drinking water for 6 days. ( b ) Rectal bleeding (Left) and stool consistency (Right) were scored daily. ( c ) Survival of the indicated miR-148a bone marrow chimera mice after DSS treatment. ( d ) Colon length from indicated miR-148a bone marrow chimera mice on day 9 after DSS treatment. ( e ) Activation of NF- κ B and STAT3 signaling in colon tissues was determined by immuno-blotting on day 9. Each lane represents an individual mouse. ( f ) mRNA (Top) and protein (Bottom) levels of the indicated cytokines were determined by reverse transcription quantitative-PCR and ELISA, respectively, in colon tissues on day 9. ( g ) Colon tissues on day 9 after DSS treatment were fixed, stained with hematoxylin and eosin (H E; Left) and immuno-stained for the macrophage marker F4/80 (Right). Scale bars, 100 μ m. ( h ) Typical images of colon tumors from the indicated miR-148a bone marrow chimera mice 120 days after AOM/DSS treatment. ( h – k ) miR-148a bone marrow chimera mice were injected with AOM on day 0 and treated with three rounds of 2.5% DSS in drinking water for 7 days. ( i and j ) Colon tumor number ( i , Left), averge tumor volume ( i , right) and size ( j ) in the indicated miR-148a bone marrow chimera mice 120 days after AOM/DSS treatment. ( k ) Colon weight from mice in panel ( i ). Data indicate the mean±S.D. in panels ( a , b , f and j ). * P

    Article Snippet: The DSS and AOM/DSS-induced colitis and CAC mouse models followed previously described protocols., Briefly, for colitis, WT or miR-148a KO mice were provided with 3.5% DSS (216011080, MW=36-50KD; MP Biomedicals, Santa Ana, CA, USA) in drinking water for 6 days, followed by regular drinking water.

    Techniques: Expressing, Mouse Assay, Activation Assay, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Staining, Marker, Injection