dss  (Valiant)

 
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    Name:
    Dextran sodium sulfate
    Description:
    Dextran sulfate is a polyanionic derivative of dextran produced by esterification of Dextran with chlorosulphonic acid The sulfur content is approximately 17 which corresponds to an average of 1 9 sulfate groups per glucosyl residue of the dextran molecule Dextran sulfate sodium DSS is the sodium salt which is a white to off white powder freely soluble in water and salt solutions to form a stable clear solution The high purity and reproducible quality enables its application in pharmaceuticals and biotechnology industry
    Catalog Number:
    02101518-CF
    Price:
    None
    Category:
    Life Sciences Biochemicals Carbohydrates Polysaccharides
    Applications:
    Immunology, Antiviral, Anticoagulant
    Buy from Supplier


    Structured Review

    Valiant dss
    Biochemical evaluation of the effects of Escherichia coli Nissle 1917 <t>(EcN);</t> mRNA expression of cytokines (A) IL-1β, (B) IL-12, (C) TGF-β, and (D) ICAM-1 was quantified by real-time PCR, and fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), <t>DSS-colitic</t> group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Dextran sulfate is a polyanionic derivative of dextran produced by esterification of Dextran with chlorosulphonic acid The sulfur content is approximately 17 which corresponds to an average of 1 9 sulfate groups per glucosyl residue of the dextran molecule Dextran sulfate sodium DSS is the sodium salt which is a white to off white powder freely soluble in water and salt solutions to form a stable clear solution The high purity and reproducible quality enables its application in pharmaceuticals and biotechnology industry
    https://www.bioz.com/result/dss/product/Valiant
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dss - by Bioz Stars, 2021-05
    98/100 stars

    Images

    1) Product Images from "The Administration of Escherichia coli Nissle 1917 Ameliorates Development of DSS-Induced Colitis in Mice"

    Article Title: The Administration of Escherichia coli Nissle 1917 Ameliorates Development of DSS-Induced Colitis in Mice

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00468

    Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); mRNA expression of cytokines (A) IL-1β, (B) IL-12, (C) TGF-β, and (D) ICAM-1 was quantified by real-time PCR, and fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Figure Legend Snippet: Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); mRNA expression of cytokines (A) IL-1β, (B) IL-12, (C) TGF-β, and (D) ICAM-1 was quantified by real-time PCR, and fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Estimation of the phylogenetic diversity of the gut microbiota found in the different experimental groups; non-colitic ( n = 3), DSS-colitic ( n = 4), and Escherichia coli Nissle 1917 (EcN; n = 3) using the (A) Chao richness, (B) Shannon diversity, and (C) Pielou evenness. The values are means, and error bars with different letters are significantly different ( p
    Figure Legend Snippet: Estimation of the phylogenetic diversity of the gut microbiota found in the different experimental groups; non-colitic ( n = 3), DSS-colitic ( n = 4), and Escherichia coli Nissle 1917 (EcN; n = 3) using the (A) Chao richness, (B) Shannon diversity, and (C) Pielou evenness. The values are means, and error bars with different letters are significantly different ( p

    Techniques Used:

    Escherichia coli Nissle 1917 (EcN) treatment promotes recovery of DSS-induced intestinal injury and inflammation in mice. (A) Histological images of colonic tissue stained with hematoxylin and eosin showing the effect of EcN on DSS-induced colitis. Representative images of each experimental group are shown: non-colitic, DSS-colitic, and EcN. In non-colitic mice, the images show the normal appearance of the intact mucosa containing the crypts with goblet cells full of mucin. In DSS-colitic group, the images show changes in the mucosa with areas of ulceration on the epithelial layer, in addition to a lower number of goblet cells which were depleted in mucin and an intense inflammatory cell infiltrate. In EcN group, an improvement of the colonic histology is found, with a reduced area of ulceration, mostly in process of recovery, presence of goblet cells replenished with their mucin content and reduced inflammatory cell infiltrate. (B) Histological scores calculated after microscopic analyses of longitudinal colon sections. Results are expressed as mean ± SEM. Statistical significance among groups was evaluated by one-way ANOVA followed by the Tukey’s test. Different letters denote significant differences between groups ( p
    Figure Legend Snippet: Escherichia coli Nissle 1917 (EcN) treatment promotes recovery of DSS-induced intestinal injury and inflammation in mice. (A) Histological images of colonic tissue stained with hematoxylin and eosin showing the effect of EcN on DSS-induced colitis. Representative images of each experimental group are shown: non-colitic, DSS-colitic, and EcN. In non-colitic mice, the images show the normal appearance of the intact mucosa containing the crypts with goblet cells full of mucin. In DSS-colitic group, the images show changes in the mucosa with areas of ulceration on the epithelial layer, in addition to a lower number of goblet cells which were depleted in mucin and an intense inflammatory cell infiltrate. In EcN group, an improvement of the colonic histology is found, with a reduced area of ulceration, mostly in process of recovery, presence of goblet cells replenished with their mucin content and reduced inflammatory cell infiltrate. (B) Histological scores calculated after microscopic analyses of longitudinal colon sections. Results are expressed as mean ± SEM. Statistical significance among groups was evaluated by one-way ANOVA followed by the Tukey’s test. Different letters denote significant differences between groups ( p

    Techniques Used: Mouse Assay, Staining

    Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); the expression of (A) miR-150, (B) miR-155, (C) miR-223, (D) miR-143, and (E) miR-375 was quantified by real-time PCR. Fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Figure Legend Snippet: Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); the expression of (A) miR-150, (B) miR-155, (C) miR-223, (D) miR-143, and (E) miR-375 was quantified by real-time PCR. Fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); mRNA expression of epithelial integrity proteins, (A) MUC-2, (B) MUC-3, (C) occludin (OCLN), and (D) zonula occludens-1 (ZO-1), was quantified by real-time PCR, and fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Figure Legend Snippet: Biochemical evaluation of the effects of Escherichia coli Nissle 1917 (EcN); mRNA expression of epithelial integrity proteins, (A) MUC-2, (B) MUC-3, (C) occludin (OCLN), and (D) zonula occludens-1 (ZO-1), was quantified by real-time PCR, and fold changes are expressed as means ± SEM. Non-colitic group ( n = 10), DSS-colitic group ( n = 10), and EcN group ( n = 10). Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Comparison of microbiota composition between non-colitic group ( n = 3), DSS-colitic group ( n = 4), and Escherichia coli Nissle 1917 (EcN) group ( n = 3). (A) Phylum breakdown of the most abundant bacterial communities in the different groups. Results were expressed as the mean ± SEM of the proportion of sequences and compared by one-way ANOVA followed by Tukey’s test. (B) The Firmicutes / Bacteriodetes ratio (F/B ratio) was calculated as a biomarker of gut dysbiosis. Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Figure Legend Snippet: Comparison of microbiota composition between non-colitic group ( n = 3), DSS-colitic group ( n = 4), and Escherichia coli Nissle 1917 (EcN) group ( n = 3). (A) Phylum breakdown of the most abundant bacterial communities in the different groups. Results were expressed as the mean ± SEM of the proportion of sequences and compared by one-way ANOVA followed by Tukey’s test. (B) The Firmicutes / Bacteriodetes ratio (F/B ratio) was calculated as a biomarker of gut dysbiosis. Statistical analysis was performed with one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p

    Techniques Used: Biomarker Assay

    (A) Principal component analysis plot based on Bray–Curtis distances, calculated on the metagenomic table of fecal samples of the different groups [non-colitic ( n = 3), DSS-colitic ( n = 4), and Escherichia coli Nissle 1917 (EcN; n = 3)]. (B) Mean percentage of sequences of the most important genera in DSS-induced colitis model. Results were shown as the means ± SEM and compared by one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p
    Figure Legend Snippet: (A) Principal component analysis plot based on Bray–Curtis distances, calculated on the metagenomic table of fecal samples of the different groups [non-colitic ( n = 3), DSS-colitic ( n = 4), and Escherichia coli Nissle 1917 (EcN; n = 3)]. (B) Mean percentage of sequences of the most important genera in DSS-induced colitis model. Results were shown as the means ± SEM and compared by one-way ANOVA followed by Tukey’s test. Bars with different letters are significantly different ( p

    Techniques Used:

    2) Product Images from "Multifunctional role of dextran sulfate sodium for in vivo modeling of intestinal diseases"

    Article Title: Multifunctional role of dextran sulfate sodium for in vivo modeling of intestinal diseases

    Journal: BMC Immunology

    doi: 10.1186/1471-2172-13-41

    TLR9 is important for protection against mild, but not severe intestinal injury. TLR9-deficient mice were treated with 3% (A, C, E) or 1% (B, D, F) DSS in their drinking water for seven days, then supplied with regular drinking water for seven days. Wild type mice from the same experiment are depicted in Figure 1 for comparison. Mice were scored for the presence of occult blood (A, B) and stool consistency (C, D) on a daily basis during the fourteen day experiment as described in the materials and methods. (E, F) Mice were weighed on a daily basis to calculate the percent change in weight for the treatment (days 0–7) and recovery (days 7–14) periods. One of two experiments (5–6 mice per condition) with similar results shown. *** p
    Figure Legend Snippet: TLR9 is important for protection against mild, but not severe intestinal injury. TLR9-deficient mice were treated with 3% (A, C, E) or 1% (B, D, F) DSS in their drinking water for seven days, then supplied with regular drinking water for seven days. Wild type mice from the same experiment are depicted in Figure 1 for comparison. Mice were scored for the presence of occult blood (A, B) and stool consistency (C, D) on a daily basis during the fourteen day experiment as described in the materials and methods. (E, F) Mice were weighed on a daily basis to calculate the percent change in weight for the treatment (days 0–7) and recovery (days 7–14) periods. One of two experiments (5–6 mice per condition) with similar results shown. *** p

    Techniques Used: Mouse Assay

    3) Product Images from "Tuberous sclerosis complex and Myc coordinate the growth and division of Drosophila intestinal stem cells"

    Article Title: Tuberous sclerosis complex and Myc coordinate the growth and division of Drosophila intestinal stem cells

    Journal: The Journal of Cell Biology

    doi: 10.1083/jcb.201103018

    Loss of TSC leads to impaired intestinal homeostasis. (A and B) Midgut morphology in wild-type (WT) and TSC2 RNAi flies. The dissected guts were mounted in Epon plastic, and after sectioning, the tissues were stained with Toluidine blue. In the wild-type gut, the enterocytes are more tightly packed around the lumen, and protrusions are seen in most enterocytes. In the TSC2 RNAi gut, the enterocytes still form a continuous epithelium, but there are fewer protrusions, and there are fewer enterocytes in each section. The overall gut appeared thinner and smoother. (C and D) Wild type were esg > GFP;tubulin Gal80 ts flies. Feeding experiments were performed at 29°C. Wild-type and TSC2 RNAi flies were fed with 5% sucrose as a control or with added 1% DSS or 2 µg/ml bleomycin. Flies were counted and transferred to new feeding vials every day. The survival rate is shown as a percentage. TSC2 RNAi flies have increased susceptibility toward the two tissue-damaging agents. Three independent experiments were performed with 100 flies for each sample. (E) A model for TSC coordination of ISC growth and division through the TORC1 pathway. Both TORC1 and InR pathways can stimulate growth and division but appear to act independently in adult midgut ISCs. TSC inhibits TORC1 and ISC growth. In the absence of TSC, TORC1 stimulates an excessive growth, which leads to the inhibition of ISC division. The TORC2 function is dispensable in ISC growth and division. Myc may act independently to regulate ISC growth, but reducing Myc is sufficient to suppress the excessive growth induced by loss of TSC. The arrows indicate activation, and the lines with a bar end indicates repression. Error bars are standard deviations.
    Figure Legend Snippet: Loss of TSC leads to impaired intestinal homeostasis. (A and B) Midgut morphology in wild-type (WT) and TSC2 RNAi flies. The dissected guts were mounted in Epon plastic, and after sectioning, the tissues were stained with Toluidine blue. In the wild-type gut, the enterocytes are more tightly packed around the lumen, and protrusions are seen in most enterocytes. In the TSC2 RNAi gut, the enterocytes still form a continuous epithelium, but there are fewer protrusions, and there are fewer enterocytes in each section. The overall gut appeared thinner and smoother. (C and D) Wild type were esg > GFP;tubulin Gal80 ts flies. Feeding experiments were performed at 29°C. Wild-type and TSC2 RNAi flies were fed with 5% sucrose as a control or with added 1% DSS or 2 µg/ml bleomycin. Flies were counted and transferred to new feeding vials every day. The survival rate is shown as a percentage. TSC2 RNAi flies have increased susceptibility toward the two tissue-damaging agents. Three independent experiments were performed with 100 flies for each sample. (E) A model for TSC coordination of ISC growth and division through the TORC1 pathway. Both TORC1 and InR pathways can stimulate growth and division but appear to act independently in adult midgut ISCs. TSC inhibits TORC1 and ISC growth. In the absence of TSC, TORC1 stimulates an excessive growth, which leads to the inhibition of ISC division. The TORC2 function is dispensable in ISC growth and division. Myc may act independently to regulate ISC growth, but reducing Myc is sufficient to suppress the excessive growth induced by loss of TSC. The arrows indicate activation, and the lines with a bar end indicates repression. Error bars are standard deviations.

    Techniques Used: Staining, Activated Clotting Time Assay, Inhibition, Activation Assay

    Loss of TSC causes defects in mitotic regulators and ISC division. (A) The number of days after heat shock induction of mitotic recombination in TSC2 193 mutant MARCM flies is indicated. The guts were stained for Delta. GFP+ clusters or single cells that also contained Delta were counted. If a cluster contained two or more GFP+ cells, it was counted as a multiple-cell clone. Most Delta+ MARCM cells remained as single cells. n ≥ 175. (B) The TSC2 RNAi was v6313 crossed with the esg > GFP;tubulin-Gal80 ts flies. The control guts had ∼5–10 mitotic cells after 6 or 12 d of incubation at 29°C, whereas the TSC2 RNAi guts had almost no detectable mitotic cells after a similar incubation (white bars). Feeding of DSS or bleomycin increased the mitotic cell counts in the control flies, but similar feeding could not increase mitotic cell counts in the TSC2 RNAi flies. Three independent experiments were performed, and four guts were counted for each sample. (C–D‴) The Polo-GFP is a protein trap line. The expression was detected by anti-GFP immunofluorescent staining. Most Polo-GFP+ cells also had Delta staining. In some wild-type cells, the GFP fusion is enriched at the metaphase plate (arrows in C–C‴ and inset in C’). In TSC2 RNAi flies, the Polo-GFP was still detectable in the cytoplasm of Delta+ cells, but almost none of them showed metaphase plate staining. (E–F‴) The control was esg > GFP, and Cdc2 and Delta antibodies were used for immunofluorescent staining. The arrows in these panels indicate Delta+ cells. In control guts, all Delta+ cells also had Cdc2 staining. In TSC2 RNAi guts, the esg > GFP+;Delta+ cells were larger, but they did not contain Cdc2 staining. Error bars are standard deviations. *, P
    Figure Legend Snippet: Loss of TSC causes defects in mitotic regulators and ISC division. (A) The number of days after heat shock induction of mitotic recombination in TSC2 193 mutant MARCM flies is indicated. The guts were stained for Delta. GFP+ clusters or single cells that also contained Delta were counted. If a cluster contained two or more GFP+ cells, it was counted as a multiple-cell clone. Most Delta+ MARCM cells remained as single cells. n ≥ 175. (B) The TSC2 RNAi was v6313 crossed with the esg > GFP;tubulin-Gal80 ts flies. The control guts had ∼5–10 mitotic cells after 6 or 12 d of incubation at 29°C, whereas the TSC2 RNAi guts had almost no detectable mitotic cells after a similar incubation (white bars). Feeding of DSS or bleomycin increased the mitotic cell counts in the control flies, but similar feeding could not increase mitotic cell counts in the TSC2 RNAi flies. Three independent experiments were performed, and four guts were counted for each sample. (C–D‴) The Polo-GFP is a protein trap line. The expression was detected by anti-GFP immunofluorescent staining. Most Polo-GFP+ cells also had Delta staining. In some wild-type cells, the GFP fusion is enriched at the metaphase plate (arrows in C–C‴ and inset in C’). In TSC2 RNAi flies, the Polo-GFP was still detectable in the cytoplasm of Delta+ cells, but almost none of them showed metaphase plate staining. (E–F‴) The control was esg > GFP, and Cdc2 and Delta antibodies were used for immunofluorescent staining. The arrows in these panels indicate Delta+ cells. In control guts, all Delta+ cells also had Cdc2 staining. In TSC2 RNAi guts, the esg > GFP+;Delta+ cells were larger, but they did not contain Cdc2 staining. Error bars are standard deviations. *, P

    Techniques Used: Mutagenesis, Staining, Incubation, Expressing

    TSC regulates ISC growth and division through TORC1 but not TORC2. (A) Expression of InR Ac (InR A1325D ) by the esgGal4 driver increased pH3 count. Feeding of rapamycin decreased the pH3 count by only a small fraction. n = 10. (B) Expression of InR Ac or PTEN RNAi driven by esgGal4 increased pH3 count by ∼10- and 4-fold, respectively. TSC2 RNAi suppressed the pH3 count in the midguts of wild-type (WT), InR Ac , and PTEN RNAi flies. n ≥ 12. (C) The pH3 count in wild-type and mutant guts with or without feeding tissue-damaging agents (DSS and bleomycin). The wild-type, sin1 /deficiency, and ric1/ric2 fly guts all showed an increase in pH3 count after tissue damage. In contrast, the TSC2 RNAi fly guts showed highly reduced mitotic count in all conditions. Four independent experiments were performed, and four guts were examined for each sample. (D) Western blots showing the C-terminal phosphorylation of AKT in various genetic backgrounds. There was a substantial reduction of AKT phosphorylation in sin1 and rictor mutant flies and guts. However, the TSC2 RNAi flies and guts showed similar AKT phosphorylation as wild type. The TSC2 RNAi was driven by the esgGal4. (E) esg > GFP;tubulin-Gal80 ts flies were used as wild type. Feeding with DSS increased the pH3 count, whereas inclusion of DMSO or rapamycin in the food did not change the mitotic count in wild-type flies. Similar feeding experiments with TSC2 RNAi flies showed that adding rapamycin at the beginning of the experiment (day 0) restored the mitotic activity. (F) A similar rapamycin and DMSO feeding experiment as in E with the exception that the rapamycin and DMSO were included in the food at day 5 after shifting the temperature to 29°C to initiate the TSC2 RNAi. This late rapamycin treatment did not restore the pH3 count. (E and F) Three independent experiments were performed, and four guts were examined for each sample. Error bars are standard deviations. **, P
    Figure Legend Snippet: TSC regulates ISC growth and division through TORC1 but not TORC2. (A) Expression of InR Ac (InR A1325D ) by the esgGal4 driver increased pH3 count. Feeding of rapamycin decreased the pH3 count by only a small fraction. n = 10. (B) Expression of InR Ac or PTEN RNAi driven by esgGal4 increased pH3 count by ∼10- and 4-fold, respectively. TSC2 RNAi suppressed the pH3 count in the midguts of wild-type (WT), InR Ac , and PTEN RNAi flies. n ≥ 12. (C) The pH3 count in wild-type and mutant guts with or without feeding tissue-damaging agents (DSS and bleomycin). The wild-type, sin1 /deficiency, and ric1/ric2 fly guts all showed an increase in pH3 count after tissue damage. In contrast, the TSC2 RNAi fly guts showed highly reduced mitotic count in all conditions. Four independent experiments were performed, and four guts were examined for each sample. (D) Western blots showing the C-terminal phosphorylation of AKT in various genetic backgrounds. There was a substantial reduction of AKT phosphorylation in sin1 and rictor mutant flies and guts. However, the TSC2 RNAi flies and guts showed similar AKT phosphorylation as wild type. The TSC2 RNAi was driven by the esgGal4. (E) esg > GFP;tubulin-Gal80 ts flies were used as wild type. Feeding with DSS increased the pH3 count, whereas inclusion of DMSO or rapamycin in the food did not change the mitotic count in wild-type flies. Similar feeding experiments with TSC2 RNAi flies showed that adding rapamycin at the beginning of the experiment (day 0) restored the mitotic activity. (F) A similar rapamycin and DMSO feeding experiment as in E with the exception that the rapamycin and DMSO were included in the food at day 5 after shifting the temperature to 29°C to initiate the TSC2 RNAi. This late rapamycin treatment did not restore the pH3 count. (E and F) Three independent experiments were performed, and four guts were examined for each sample. Error bars are standard deviations. **, P

    Techniques Used: Expressing, Mutagenesis, Western Blot, Activity Assay

    4) Product Images from "Ras Guanine Nucleotide-releasing Protein-4 (RasGRP4) Involvement in Experimental Arthritis and Colitis *"

    Article Title: Ras Guanine Nucleotide-releasing Protein-4 (RasGRP4) Involvement in Experimental Arthritis and Colitis *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.360388

    RasGRP4 deficiency abrogates acute DSS-induced colitis. A , percent weight loss in the DSS model of acute inflammatory colitis. DSS-treated WT mice (+/+) lost significantly more weight (*, p
    Figure Legend Snippet: RasGRP4 deficiency abrogates acute DSS-induced colitis. A , percent weight loss in the DSS model of acute inflammatory colitis. DSS-treated WT mice (+/+) lost significantly more weight (*, p

    Techniques Used: Mouse Assay

    5) Product Images from "Loss of PACS-2 delays regeneration in DSS-induced colitis but does not affect the ApcMin model of colorectal cancer"

    Article Title: Loss of PACS-2 delays regeneration in DSS-induced colitis but does not affect the ApcMin model of colorectal cancer

    Journal: Oncotarget

    doi: 10.18632/oncotarget.22661

    Pacs2 -/- mice show comparable inflammation and tissue damage during DSS-induced colitis Histological sections were scored blindly using the criteria outlined in Table 2 . A. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10. Scale bar overview pictures = 1 mm. Scale bar detail figures = 0.1 mm. B. Dot plots show the histology score, calculated as the sum of the epithelial damage score and the inflammation score. The individual scores were calculated as described in Table 2 . All data represent the mean ± S.E.M. and were analyzed by unpaired Student’s t-test ( n = 6-13 as indicated). Data were pooled from three independent experiments.
    Figure Legend Snippet: Pacs2 -/- mice show comparable inflammation and tissue damage during DSS-induced colitis Histological sections were scored blindly using the criteria outlined in Table 2 . A. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10. Scale bar overview pictures = 1 mm. Scale bar detail figures = 0.1 mm. B. Dot plots show the histology score, calculated as the sum of the epithelial damage score and the inflammation score. The individual scores were calculated as described in Table 2 . All data represent the mean ± S.E.M. and were analyzed by unpaired Student’s t-test ( n = 6-13 as indicated). Data were pooled from three independent experiments.

    Techniques Used: Mouse Assay, Isolation

    Evaluation of the regenerative response of intestinal epithelial cells in DSS-treated Pacs2 -/- mice A. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for phosphorylated EGFR (Tyr1068) and nuclear DAPI stain. B. The graph shows the pEGFR fluorescence intensity quantified along a line across colonic crypts (represented by the dotted line in A) on 5 equally positioned, random confocal images from each of 5 control and 5 Pacs2-/- mice. C. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for Ki67 positive proliferating cells. D. The graph shows Ki67 positive cells represented as the percentage diaminobenzidine (DAB) positive area per total hematoxylin stained nuclear area from 5 equally positioned, random images from each of 5 control and 5 Pacs2-/- mice. E. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for apoptotic cells by ApopTag. F. The graph shows the number of apoptotic cells per mm 2 counted from 3 equally positioned, random images from each of 5 control and 5 Pacs2-/- mice. Scale bars = 50 µm. All graphs show mean values ± SEM analyzed by unpaired two-tailed Student’s t-test. ** p
    Figure Legend Snippet: Evaluation of the regenerative response of intestinal epithelial cells in DSS-treated Pacs2 -/- mice A. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for phosphorylated EGFR (Tyr1068) and nuclear DAPI stain. B. The graph shows the pEGFR fluorescence intensity quantified along a line across colonic crypts (represented by the dotted line in A) on 5 equally positioned, random confocal images from each of 5 control and 5 Pacs2-/- mice. C. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for Ki67 positive proliferating cells. D. The graph shows Ki67 positive cells represented as the percentage diaminobenzidine (DAB) positive area per total hematoxylin stained nuclear area from 5 equally positioned, random images from each of 5 control and 5 Pacs2-/- mice. E. Representative images of colonic specimens from control and Pacs2 -/- mice isolated at day 6 and day 10 and stained for apoptotic cells by ApopTag. F. The graph shows the number of apoptotic cells per mm 2 counted from 3 equally positioned, random images from each of 5 control and 5 Pacs2-/- mice. Scale bars = 50 µm. All graphs show mean values ± SEM analyzed by unpaired two-tailed Student’s t-test. ** p

    Techniques Used: Mouse Assay, Isolation, Staining, Fluorescence, Two Tailed Test

    Pacs2 -/- mice show no significant changes in susceptibility to DSS-induced colitis A. Schematic of the DSS treatment regimen and data collection. Littermate Pacs2 +/+ (control, n = 21) and Pacs2 -/- ( n = 17) mice received 2.3% DSS in their drinking water for five days, followed by five days on regular water. Mice were weighed on days 0, 2, and 5-10, and stool consistency and blood content additionally monitored from days 5-10. B. Quantitative real-time PCR analysis of Pacs2 and Pacs1 mRNA levels in the colon of control ( n = 5) and Pacs2 -/- mice ( n = 4). Gapdh served as a control for normalization. C. Quantitative real-time PCR analysis of Pacs2 mRNA levels in colonic tissue isolated from Pacs2 +/+ mice at Day 0, 6 and 10 during DSS-induced colitis. D. Kaplan-Meier plot depicting the percentage survival of control (61 %) versus Pacs2 -/- (35 %) mice. Survival was evaluated by log-rank (Mantel-Cox) test (control, n = 21; Pacs2 -/- , n = 17). E. Changes in colon length in control and Pacs2 -/- mice on day 6 of the DSS protocol (control, n = 9; Pacs2 -/- , n = 4). F. Daily changes in body weight during DSS-induced colitis. Changes in body weight percentage were calculated by normalizing body weight at the specific day to the body weight at day 0 (control, n = 21; Pacs2 -/- , n = 17). G. The Disease Activity Index (DAI) was calculated as the average of the weight loss score, stool score, and bleeding scores (control, n = 21; Pacs2 -/- , n = 17). All data were pooled from three independent experiments. Graphs represent the mean ± S.E.M; *** p
    Figure Legend Snippet: Pacs2 -/- mice show no significant changes in susceptibility to DSS-induced colitis A. Schematic of the DSS treatment regimen and data collection. Littermate Pacs2 +/+ (control, n = 21) and Pacs2 -/- ( n = 17) mice received 2.3% DSS in their drinking water for five days, followed by five days on regular water. Mice were weighed on days 0, 2, and 5-10, and stool consistency and blood content additionally monitored from days 5-10. B. Quantitative real-time PCR analysis of Pacs2 and Pacs1 mRNA levels in the colon of control ( n = 5) and Pacs2 -/- mice ( n = 4). Gapdh served as a control for normalization. C. Quantitative real-time PCR analysis of Pacs2 mRNA levels in colonic tissue isolated from Pacs2 +/+ mice at Day 0, 6 and 10 during DSS-induced colitis. D. Kaplan-Meier plot depicting the percentage survival of control (61 %) versus Pacs2 -/- (35 %) mice. Survival was evaluated by log-rank (Mantel-Cox) test (control, n = 21; Pacs2 -/- , n = 17). E. Changes in colon length in control and Pacs2 -/- mice on day 6 of the DSS protocol (control, n = 9; Pacs2 -/- , n = 4). F. Daily changes in body weight during DSS-induced colitis. Changes in body weight percentage were calculated by normalizing body weight at the specific day to the body weight at day 0 (control, n = 21; Pacs2 -/- , n = 17). G. The Disease Activity Index (DAI) was calculated as the average of the weight loss score, stool score, and bleeding scores (control, n = 21; Pacs2 -/- , n = 17). All data were pooled from three independent experiments. Graphs represent the mean ± S.E.M; *** p

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

    6) Product Images from "Mast cells are essential intermediaries in regulating IL-33/ST2 signaling for an immune network favorable to mucosal healing in experimentally inflamed colons"

    Article Title: Mast cells are essential intermediaries in regulating IL-33/ST2 signaling for an immune network favorable to mucosal healing in experimentally inflamed colons

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-018-1223-4

    KIT Wsh mice fail in timely recovery from colitis due to MC deficiency. a Alterations in body weight as the percentage of initial weight at the start of experiments during a 15-day observation (24 WT mice and 14 KIT Wsh mice). b Survival rate for WT and KIT Wsh mice after DSS insult. c Whole colon lengths from sham, activation phase, and remission phase. d Disease score evaluated as weight loss, feces, rectal bleeding, and general appearance as indicated. e Representative H E staining images of transverse colon. f Pathological scores from colonic sections, calculated as indicated. g Serum FITC-dextran quantified as a measure of intestinal permeability. h Percentage of positive cells for Ki-67 immunostaining. i Representative stain of Ki-67. j Heat map of relative transcriptional level of selected mRNA involved in mucosal recovery and homeostasis maintenance. Data are mean ± SD. Student t- test, * P
    Figure Legend Snippet: KIT Wsh mice fail in timely recovery from colitis due to MC deficiency. a Alterations in body weight as the percentage of initial weight at the start of experiments during a 15-day observation (24 WT mice and 14 KIT Wsh mice). b Survival rate for WT and KIT Wsh mice after DSS insult. c Whole colon lengths from sham, activation phase, and remission phase. d Disease score evaluated as weight loss, feces, rectal bleeding, and general appearance as indicated. e Representative H E staining images of transverse colon. f Pathological scores from colonic sections, calculated as indicated. g Serum FITC-dextran quantified as a measure of intestinal permeability. h Percentage of positive cells for Ki-67 immunostaining. i Representative stain of Ki-67. j Heat map of relative transcriptional level of selected mRNA involved in mucosal recovery and homeostasis maintenance. Data are mean ± SD. Student t- test, * P

    Techniques Used: Mouse Assay, Activation Assay, Staining, Permeability, Immunostaining

    Comparison during DSS-induced colitis between WT, KIT Wsh , and KIT Wsh reconstituted mice. a Flow cytometric evaluation of the purity of BMMC preparation. Three different experiments were repeated. b Identification of MC presence in the colon tissue of reconstituted KIT Wsh mice by using toluidine blue staining (8 KIT Wsh mice were used). c Percent difference of body mass from day 0 between different groups (KIT Wsh + MCs mice: n = 8; KIT Wsh mice: n = 24; WT mice: n = 31). d Survival rate of WT and KIT Wsh , and reconstituted KIT Wsh mice after DSS insult. e Whole colon lengths from sham, activation phase, and remission phase. f Disease score evaluated as weight loss, feces, rectal bleeding, and general appearance as indicated. g Pathological scores from colonic sections, calculated as indicated. h Representative H E staining images of transverse colon at day 14. Data are mean ± SD. Student t- test, * P
    Figure Legend Snippet: Comparison during DSS-induced colitis between WT, KIT Wsh , and KIT Wsh reconstituted mice. a Flow cytometric evaluation of the purity of BMMC preparation. Three different experiments were repeated. b Identification of MC presence in the colon tissue of reconstituted KIT Wsh mice by using toluidine blue staining (8 KIT Wsh mice were used). c Percent difference of body mass from day 0 between different groups (KIT Wsh + MCs mice: n = 8; KIT Wsh mice: n = 24; WT mice: n = 31). d Survival rate of WT and KIT Wsh , and reconstituted KIT Wsh mice after DSS insult. e Whole colon lengths from sham, activation phase, and remission phase. f Disease score evaluated as weight loss, feces, rectal bleeding, and general appearance as indicated. g Pathological scores from colonic sections, calculated as indicated. h Representative H E staining images of transverse colon at day 14. Data are mean ± SD. Student t- test, * P

    Techniques Used: Mouse Assay, Flow Cytometry, Staining, Activation Assay

    7) Product Images from "The IL-33/ST2 pathway shapes the regulatory T cell phenotype to promote intestinal cancer"

    Article Title: The IL-33/ST2 pathway shapes the regulatory T cell phenotype to promote intestinal cancer

    Journal: Mucosal Immunology

    doi: 10.1038/s41385-019-0176-y

    IL-33 restrains IL-17 production in CD4 + T cells. a Foxp3 /eGFP mice were treated with AOM/DSS and eGFP + CD4 + T cells were isolated from CRC lesions for transcriptomic analysis. Heat map showing all genes in the gene ontology pathway “Th17 cell differentiation” (ko04659) that are differentially expressed in ST2 + versus ST2 − eGFP + Tregs isolated from CRC lesions from the indicated four mice (adjusted p -value p ≤ 0.05). Blue indicates higher transcript expression in ST2 − Tregs and yellow/red higher expression in ST2 + Tregs. BALB/c mice were treated with AOM/DSS and FOXP3 − CD4 + T cells b or FOXP3 + CD4 + Tregs c were analyzed in the intestine for ST2 and IL-17 expression. Shown are flow cytometry plots from each one representative sample out of three. d–h Sort-purified eGFP + b , c or eGFP − d , f CD4 + T cells from spleens of naïve Foxp3 /eGFP reporter mice were stimulated with anti-CD3/anti-CD28 antibodies (ctrl) or cultured under Th17 polarizing conditions in the presence or absence of IL-33. d Frequencies of ST2-positive or e IL-17A-positive cells were measured among CD4 + FOXP3 + Tregs. f Flow cytometry plots from one representative experiment showing the gating strategy applied to assess the proportion of IL-17A-expressing cells among FOXP3 + (right upper panel) or FOXP3 - CD4 + T cells (right lower panel). In this particular dataset, eGFP − CD4 + T were cultured under Th17-polarizing conditions, in the presence of IL-33. Frequencies of IL-17A-expressing cells were measured among g CD4 + FOXP3 + Tregs or FOXP3 − CD4 + T cells h . d , e Data are mean ± SEM and were pooled from two representative experiment ( n = 6 mice). Statistical analyses were performed using paired Student’s t -test. g , h Data are mean ± SEM ( n = 10 mice, pooled from three independent experiments) and statistical analyses were performed using Wilcoxon matched-pairs signed rank test. * P
    Figure Legend Snippet: IL-33 restrains IL-17 production in CD4 + T cells. a Foxp3 /eGFP mice were treated with AOM/DSS and eGFP + CD4 + T cells were isolated from CRC lesions for transcriptomic analysis. Heat map showing all genes in the gene ontology pathway “Th17 cell differentiation” (ko04659) that are differentially expressed in ST2 + versus ST2 − eGFP + Tregs isolated from CRC lesions from the indicated four mice (adjusted p -value p ≤ 0.05). Blue indicates higher transcript expression in ST2 − Tregs and yellow/red higher expression in ST2 + Tregs. BALB/c mice were treated with AOM/DSS and FOXP3 − CD4 + T cells b or FOXP3 + CD4 + Tregs c were analyzed in the intestine for ST2 and IL-17 expression. Shown are flow cytometry plots from each one representative sample out of three. d–h Sort-purified eGFP + b , c or eGFP − d , f CD4 + T cells from spleens of naïve Foxp3 /eGFP reporter mice were stimulated with anti-CD3/anti-CD28 antibodies (ctrl) or cultured under Th17 polarizing conditions in the presence or absence of IL-33. d Frequencies of ST2-positive or e IL-17A-positive cells were measured among CD4 + FOXP3 + Tregs. f Flow cytometry plots from one representative experiment showing the gating strategy applied to assess the proportion of IL-17A-expressing cells among FOXP3 + (right upper panel) or FOXP3 - CD4 + T cells (right lower panel). In this particular dataset, eGFP − CD4 + T were cultured under Th17-polarizing conditions, in the presence of IL-33. Frequencies of IL-17A-expressing cells were measured among g CD4 + FOXP3 + Tregs or FOXP3 − CD4 + T cells h . d , e Data are mean ± SEM and were pooled from two representative experiment ( n = 6 mice). Statistical analyses were performed using paired Student’s t -test. g , h Data are mean ± SEM ( n = 10 mice, pooled from three independent experiments) and statistical analyses were performed using Wilcoxon matched-pairs signed rank test. * P

    Techniques Used: Mouse Assay, Isolation, Cell Differentiation, Expressing, Flow Cytometry, Purification, Cell Culture

    Increased frequencies of effector CD8 + T cells in CRC lesions of St2 −/− mice lead to improved antitumor immunity. Mice were treated with AOM/DSS and immune cells were analyzed in CRC lesions (CRC) or in adjacent tumor-free colons (ctrl). a Frequencies of CD8 + T cells were correlated with frequencies of ST2 + CD4 + Tregs in WT tumor tissues ( n = 47 mice, pooled from nine independent experiments). b Frequencies of CD8 + T cells were measured in the intestine of the indicated strains. c Flow cytometry plots from one representative mouse per group depicted in d or e showing CRC-derived CD8 + T cells expressing IFNγ or GZMB, respectively. d Frequencies of IFNγ– or e GZMB-expressing CD8 + T cells were measured in the intestine of the indicated strains. f Median fluorescence intensity (MFI) of GZMB was measured on CRC-derived CD8 + T cells. g Mice were treated with AOM/DSS with or without antibody-mediated CD8 + T cell depletion, as shown in this experimental setup; h colonoscopy was then performed for longitudinal assessment of the tumor score in the indicated groups, at the indicated time points after the first AOM injection. Data are mean ± SEM. Data in b–f depict one representative out of six independent experiments ( n = 4–5 mice per group) and data in h show one out of two experiments. Correlation in a was performed using Spearman correlation analysis and statistical analyses were performed using b–f standard Student’s t- test or h two-way ANOVA followed by uncorrected Fisher's LSD test. Statistics in h are shown only for the last colonoscopy time point. * P
    Figure Legend Snippet: Increased frequencies of effector CD8 + T cells in CRC lesions of St2 −/− mice lead to improved antitumor immunity. Mice were treated with AOM/DSS and immune cells were analyzed in CRC lesions (CRC) or in adjacent tumor-free colons (ctrl). a Frequencies of CD8 + T cells were correlated with frequencies of ST2 + CD4 + Tregs in WT tumor tissues ( n = 47 mice, pooled from nine independent experiments). b Frequencies of CD8 + T cells were measured in the intestine of the indicated strains. c Flow cytometry plots from one representative mouse per group depicted in d or e showing CRC-derived CD8 + T cells expressing IFNγ or GZMB, respectively. d Frequencies of IFNγ– or e GZMB-expressing CD8 + T cells were measured in the intestine of the indicated strains. f Median fluorescence intensity (MFI) of GZMB was measured on CRC-derived CD8 + T cells. g Mice were treated with AOM/DSS with or without antibody-mediated CD8 + T cell depletion, as shown in this experimental setup; h colonoscopy was then performed for longitudinal assessment of the tumor score in the indicated groups, at the indicated time points after the first AOM injection. Data are mean ± SEM. Data in b–f depict one representative out of six independent experiments ( n = 4–5 mice per group) and data in h show one out of two experiments. Correlation in a was performed using Spearman correlation analysis and statistical analyses were performed using b–f standard Student’s t- test or h two-way ANOVA followed by uncorrected Fisher's LSD test. Statistics in h are shown only for the last colonoscopy time point. * P

    Techniques Used: Mouse Assay, Flow Cytometry, Derivative Assay, Expressing, Fluorescence, Injection

    The IL-33/ST2 pathway is upregulated in intestinal tumors. Mice were treated with AOM/DSS and cancerous colonic tissues (CRC) were isolated for analysis after 10–12 weeks or at the indicated time points. Unless otherwise indicated, colon tissues from naïve mice of the corresponding strain were used as control (ctrl). Il33 transcript levels (left panel) and IL-33 protein secretion from explant cultures (right panel) were measured in the colon of a C57BL/6 mice ( n = 6–17 mice per group; data pooled from two, respectively, four independent experiments) or b BALB/c mice ( n = 10–26 mice per group; data pooled from three, respectively, five independent experiments). c Il-33 transcript levels were measured in tumor tissues of BALB/c mice at the indicated time points after the first AOM injection. Ctrl, n = 21; CRC, n = 3-6 mice per group; data are from two experiments. Transcript levels of d sSt2 and e St2 were measured in tumor lesions (CRC, n = 8 mice per group) or adjacent tumor-free tissues (ctrl, n = 7 mice per group) from C57BL/6 mice. Data are from one experiment. Data are mean ± SEM. Statistical analyses were performed using a , b , d , e standard Student’s t- test or c one-way ANOVA with Dunnett’s post-test. * P
    Figure Legend Snippet: The IL-33/ST2 pathway is upregulated in intestinal tumors. Mice were treated with AOM/DSS and cancerous colonic tissues (CRC) were isolated for analysis after 10–12 weeks or at the indicated time points. Unless otherwise indicated, colon tissues from naïve mice of the corresponding strain were used as control (ctrl). Il33 transcript levels (left panel) and IL-33 protein secretion from explant cultures (right panel) were measured in the colon of a C57BL/6 mice ( n = 6–17 mice per group; data pooled from two, respectively, four independent experiments) or b BALB/c mice ( n = 10–26 mice per group; data pooled from three, respectively, five independent experiments). c Il-33 transcript levels were measured in tumor tissues of BALB/c mice at the indicated time points after the first AOM injection. Ctrl, n = 21; CRC, n = 3-6 mice per group; data are from two experiments. Transcript levels of d sSt2 and e St2 were measured in tumor lesions (CRC, n = 8 mice per group) or adjacent tumor-free tissues (ctrl, n = 7 mice per group) from C57BL/6 mice. Data are from one experiment. Data are mean ± SEM. Statistical analyses were performed using a , b , d , e standard Student’s t- test or c one-way ANOVA with Dunnett’s post-test. * P

    Techniques Used: Mouse Assay, Isolation, Injection

    ST2 is preferentially upregulated on CD4 + FOXP3 + Tregs in intestinal tumors. Mice were treated with AOM/DSS (CRC; black bars) or left untreated (ctrl; white bars), and immune cells from spleen, mesenteric lymph nodes (mLN), or colon were analyzed by flow cytometry. a Frequencies of ST2-positive cells were measured among CD4 + T cells, CD8 + T cells, B220 + B cells, GR1 + granulocytes, F4/80 + CD11c int/− macrophages (Mph), CD11c + F4/80 − dendritic cells (DC) and CD335 + NK cells, respectively ( n = 7–8 BALB/c mice per group). Frequencies of ST2-positive cells were measured among FOXP3 − (left panel) or FOXP3 + (right panel) CD4 + T cells from b BALB/c ( n = 15–22 mice per group) or c C57BL/6- Foxp3 /RFP mice ( n = 10–16 mice per group). d Frequencies of ST2 + FOXP3 + Tregs were measured in CRC lesions of BALB/c mice at the indicated time points during AOM/DSS treatment ( n = 26 for ctrl and n = 7–11 for CRC mice per time point). FOXP3 + Treg frequencies (left panel), ST2-expressing FOXP3 + Treg frequencies (middle panel), or IL-33 protein expression (right panel) in colon were correlated with tumor score in e BALB/c ( n = 16-28) or f C57BL/6- Foxp3 /RFP ( n = 14–31) mice. g Alternatively, Apc +/1638N mice ( n = 13) were analyzed at different ages and frequencies of ST2-expressing FOXP3 + Treg were correlated with tumor numbers in the colon. h Msh2 fl/fl ; Villin-Cre mice ( n = 11) were analyzed 269–342 days after birth and frequencies of ST2-expressing FOXP3 + Treg were correlated with tumor weight in the small intestine. Data are mean ± SEM and were pooled from a , h two, b , c four, d three, e 4–5, f 3–7 or g several independent experiments. Statistical analyses were performed using a–c two-way ANOVA with Sidak post-test and d one-way ANOVA with Dunnett's post-test. Correlations were calculated using Spearman correlation analysis. * P
    Figure Legend Snippet: ST2 is preferentially upregulated on CD4 + FOXP3 + Tregs in intestinal tumors. Mice were treated with AOM/DSS (CRC; black bars) or left untreated (ctrl; white bars), and immune cells from spleen, mesenteric lymph nodes (mLN), or colon were analyzed by flow cytometry. a Frequencies of ST2-positive cells were measured among CD4 + T cells, CD8 + T cells, B220 + B cells, GR1 + granulocytes, F4/80 + CD11c int/− macrophages (Mph), CD11c + F4/80 − dendritic cells (DC) and CD335 + NK cells, respectively ( n = 7–8 BALB/c mice per group). Frequencies of ST2-positive cells were measured among FOXP3 − (left panel) or FOXP3 + (right panel) CD4 + T cells from b BALB/c ( n = 15–22 mice per group) or c C57BL/6- Foxp3 /RFP mice ( n = 10–16 mice per group). d Frequencies of ST2 + FOXP3 + Tregs were measured in CRC lesions of BALB/c mice at the indicated time points during AOM/DSS treatment ( n = 26 for ctrl and n = 7–11 for CRC mice per time point). FOXP3 + Treg frequencies (left panel), ST2-expressing FOXP3 + Treg frequencies (middle panel), or IL-33 protein expression (right panel) in colon were correlated with tumor score in e BALB/c ( n = 16-28) or f C57BL/6- Foxp3 /RFP ( n = 14–31) mice. g Alternatively, Apc +/1638N mice ( n = 13) were analyzed at different ages and frequencies of ST2-expressing FOXP3 + Treg were correlated with tumor numbers in the colon. h Msh2 fl/fl ; Villin-Cre mice ( n = 11) were analyzed 269–342 days after birth and frequencies of ST2-expressing FOXP3 + Treg were correlated with tumor weight in the small intestine. Data are mean ± SEM and were pooled from a , h two, b , c four, d three, e 4–5, f 3–7 or g several independent experiments. Statistical analyses were performed using a–c two-way ANOVA with Sidak post-test and d one-way ANOVA with Dunnett's post-test. Correlations were calculated using Spearman correlation analysis. * P

    Techniques Used: Mouse Assay, Flow Cytometry, Expressing

    ST2 expression shapes the transcriptome and the phenotype of tumor-derived FOXP3 + Tregs. Foxp3 /eGFP mice were treated with AOM/DSS and eGFP + CD4 + T cells from CRC lesions were sort-purified into ST2 + versus ST2 − cells for microarray analysis. a Principal component analysis depicting matched samples, connected by lines, from four analyzed mice. b Pathway analysis showing 58 pathways that were found to be differentially regulated between ST2 + versus ST2 − eGFP + CD4 + T cells (with adjusted p -value p
    Figure Legend Snippet: ST2 expression shapes the transcriptome and the phenotype of tumor-derived FOXP3 + Tregs. Foxp3 /eGFP mice were treated with AOM/DSS and eGFP + CD4 + T cells from CRC lesions were sort-purified into ST2 + versus ST2 − cells for microarray analysis. a Principal component analysis depicting matched samples, connected by lines, from four analyzed mice. b Pathway analysis showing 58 pathways that were found to be differentially regulated between ST2 + versus ST2 − eGFP + CD4 + T cells (with adjusted p -value p

    Techniques Used: Expressing, Derivative Assay, Mouse Assay, Purification, Microarray

    Treg frequencies are reduced in tumors of St2 −/− mice. Wild-type (WT) or St2 −/− C57BL/6 mice were treated with AOM/DSS (CRC) or left untreated (ctrl) and a frequencies of CD4 + T cells in colonic tissues were measured after 10 weeks ( n = 4–20 mice per group). b Flow cytometry plots from one representative CRC mouse per group depicted in c showing frequencies of CD4 + FOXP3 + Tregs (panels on the left) and frequencies of ST2-expressing cells among FOXP3 + Tregs (panels on the right). c Frequencies of FOXP3 + Treg were measured among CD4 + T cells based on the gating strategy shown in b . d Absolute numbers of FOXP3 + Treg were measured in the colon of AOM/DSS-treated mice ( n = 8–9 mice per group). e Tumor numbers and tumor load were assessed in the colon of CRC mice ( n = 5 mice per group). f Endoscopy pictures showing tumors in the distal colon from one representative CRC mouse per group depicted in e . g Hematoxylin and eosin (H E) sections displaying representative colon tumors in the indicated groups of mice. Scale bars: overview: 200 μm; inlay: 100 μm. Indicated sets of chimeric mice were treated with AOM/DSS and h frequencies of CD4 + T cells or i frequencies of CD4 + FOXP3 + Treg were measured in the indicated organs after 10–13 weeks ( n = 7–8 mice per group). j Intestinal tumorigenesis was assessed by endoscopy and k tumor development was calculated in the indicated groups of mice by subtracting tumor score on week 10 from tumor score on week 8 after the start of AOM/DSS treatment ( n = 8–9 mice per group). Data are mean ± SEM and show a , c four pooled independent experiments out of six or e one representative experiment out of three. d , h , i , k data were pooled from two independent experiments. Statistical analyses were performed using a , c–e , k standard Student’s t- test or h , i one-way ANOVA with Bonferroni post-test. * P
    Figure Legend Snippet: Treg frequencies are reduced in tumors of St2 −/− mice. Wild-type (WT) or St2 −/− C57BL/6 mice were treated with AOM/DSS (CRC) or left untreated (ctrl) and a frequencies of CD4 + T cells in colonic tissues were measured after 10 weeks ( n = 4–20 mice per group). b Flow cytometry plots from one representative CRC mouse per group depicted in c showing frequencies of CD4 + FOXP3 + Tregs (panels on the left) and frequencies of ST2-expressing cells among FOXP3 + Tregs (panels on the right). c Frequencies of FOXP3 + Treg were measured among CD4 + T cells based on the gating strategy shown in b . d Absolute numbers of FOXP3 + Treg were measured in the colon of AOM/DSS-treated mice ( n = 8–9 mice per group). e Tumor numbers and tumor load were assessed in the colon of CRC mice ( n = 5 mice per group). f Endoscopy pictures showing tumors in the distal colon from one representative CRC mouse per group depicted in e . g Hematoxylin and eosin (H E) sections displaying representative colon tumors in the indicated groups of mice. Scale bars: overview: 200 μm; inlay: 100 μm. Indicated sets of chimeric mice were treated with AOM/DSS and h frequencies of CD4 + T cells or i frequencies of CD4 + FOXP3 + Treg were measured in the indicated organs after 10–13 weeks ( n = 7–8 mice per group). j Intestinal tumorigenesis was assessed by endoscopy and k tumor development was calculated in the indicated groups of mice by subtracting tumor score on week 10 from tumor score on week 8 after the start of AOM/DSS treatment ( n = 8–9 mice per group). Data are mean ± SEM and show a , c four pooled independent experiments out of six or e one representative experiment out of three. d , h , i , k data were pooled from two independent experiments. Statistical analyses were performed using a , c–e , k standard Student’s t- test or h , i one-way ANOVA with Bonferroni post-test. * P

    Techniques Used: Mouse Assay, Flow Cytometry, Expressing

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    Article Title: Effect of Angelica sinensis Root Extract on Cancer Prevention in Different Stages of an AOM/DSS Mouse Model
    Article Snippet: Chemicals and Reagents Azoxymethane (AOM) was purchased from Sigma-Aldrich (St. Louis, MO, USA) and dextran sodium sulfate (DSS) was purchased from MP Biomedicals (Santa Ana, CA, USA).

    Mouse Assay:

    Article Title: Intestinal inflammation without weight loss decreases bone density and growth
    Article Snippet: More importantly, the DSS-treated mice lost a significant amount of bone and displayed reduced growth plate thickness, demonstrating that colitis-induced bone changes are not dependent upon weight loss. .. Male 5–6-wk-old C57BL/6 mice were given 1% (wt/vol) dextran sodium sulfate salt (DSS) (36,000–50,000 MW, MP Biomedical, Santa Anna, CA) in sterile drinking water for 15 days to induce colitis. .. This DSS concentration was chosen on the basis of pilot dose response studies (ranging from 0.1 to 5% wt/vol DSS) that revealed weight loss when 2% DSS or more was used.

    Article Title: Bacterial immunogenic α-galactosylceramide identified in the murine large intestine: dependency on diet and inflammation [S]
    Article Snippet: The mice were fed a Western type diet (WTD) (EF TD88137, ssniff special diets GmbH, Germany, containing 21.1 % fat, 14.4% polysaccharides, 34.3% sugar, and 0.21 % cholesterol) or a standard rodent diet (control; Altromin, Lage, Germany; #1310, containing 5.1% fat, 35% polysaccharides, and 5% sugar) for 7 days and euthanized afterwards by cervical dislocation. .. Induction of colitis in miceNine- to 11-week-old C57BL/6 male mice were given 2% dextran sodium sulfate (DSS) (colitis grade, molecular weight 36,000–50,000; MP Biomedicals GmbH, Eschwege, Germany) in drinking water and euthanized, respectively, after 2 or 4 days of treatment. .. Induction of colitis was verified by performing an occult blood test (Hemoccult; Beckman Coulter GmbH, Krefeld, Germany) after 4 days of exposure to DSS.

    Article Title: Gut Commensal-Induced IκBζ Expression in Dendritic Cells Influences the Th17 Response
    Article Snippet: Cells were incubated for 4 h with GolgiStop (BD) prior to end of polarization time and processed for flow cytometry analysis. .. Dextran Sodium Sulfate (DSS)-Induced Colitis in WT and Nfkbiz -/- Mice Acute DSS colitis was induced in SPF WT and Nfkbiz -/- mice by administration of 2.5% (w/v) DSS (molecular weight 36–50 kDa, MP Biomedicals) dissolved in drinking water for 7 days. .. Onset of inflammation was assessed on day 0 and on days 3–7 by monitoring body weight and disease activity index (DAI) with parameters ranging from 0–3 regarding blood in stool and on anus, stool consistency, relieving posture and appearance of fur.

    Article Title: Notch signalling regulates asymmetric division and inter-conversion between lgr5 and bmi1 expressing intestinal stem cells
    Article Snippet: For in vivo studies, DAPT was administered every 12 hours for 3 days by i.p injection in LGR5-EGFP mice, and Tamoxifen (Sigma) was administered by daily i.p injections for 5 consecutive days in POFUT-1flox/flox mice. .. For DSS treatment, LGR5-EGFP mice were administered 3% Dextran Sodium Sulfate (DSS) (MP Biomedicals) in the drinking water for 5 days, followed by plain water for 5 days. .. During the last three days of the plain water diet, mice were injected i.p. with DAPT according to the regimen described earlier.

    Molecular Weight:

    Article Title: Bacterial immunogenic α-galactosylceramide identified in the murine large intestine: dependency on diet and inflammation [S]
    Article Snippet: The mice were fed a Western type diet (WTD) (EF TD88137, ssniff special diets GmbH, Germany, containing 21.1 % fat, 14.4% polysaccharides, 34.3% sugar, and 0.21 % cholesterol) or a standard rodent diet (control; Altromin, Lage, Germany; #1310, containing 5.1% fat, 35% polysaccharides, and 5% sugar) for 7 days and euthanized afterwards by cervical dislocation. .. Induction of colitis in miceNine- to 11-week-old C57BL/6 male mice were given 2% dextran sodium sulfate (DSS) (colitis grade, molecular weight 36,000–50,000; MP Biomedicals GmbH, Eschwege, Germany) in drinking water and euthanized, respectively, after 2 or 4 days of treatment. .. Induction of colitis was verified by performing an occult blood test (Hemoccult; Beckman Coulter GmbH, Krefeld, Germany) after 4 days of exposure to DSS.

    Article Title: Gut Commensal-Induced IκBζ Expression in Dendritic Cells Influences the Th17 Response
    Article Snippet: Cells were incubated for 4 h with GolgiStop (BD) prior to end of polarization time and processed for flow cytometry analysis. .. Dextran Sodium Sulfate (DSS)-Induced Colitis in WT and Nfkbiz -/- Mice Acute DSS colitis was induced in SPF WT and Nfkbiz -/- mice by administration of 2.5% (w/v) DSS (molecular weight 36–50 kDa, MP Biomedicals) dissolved in drinking water for 7 days. .. Onset of inflammation was assessed on day 0 and on days 3–7 by monitoring body weight and disease activity index (DAI) with parameters ranging from 0–3 regarding blood in stool and on anus, stool consistency, relieving posture and appearance of fur.

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    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
    Dss, supplied by Valiant, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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).
    Dss Colitis Dss Colitis, supplied by Valiant, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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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    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

    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

    Journal: Cellular and Molecular Gastroenterology and Hepatology

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

    doi: 10.1016/j.jcmgh.2017.12.003

    Figure Lengend 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

    Article Snippet: Induction of DSS Colitis Experimental colitis was induced in 8- to 12-week-old ERα-KO, ERβ-KO, and WT littermate mice with 2.5% wt/vol DSS (molecular weight, 36,000–50,000 daltons; MP Biomedicals, Solon, OH) dissolved in sterile drinking water given ad libitum for 5 days, followed by 1 day of tap water.

    Techniques: 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.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

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

    doi: 10.1016/j.jcmgh.2017.12.003

    Figure Lengend 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.

    Article Snippet: Induction of DSS Colitis Experimental colitis was induced in 8- to 12-week-old ERα-KO, ERβ-KO, and WT littermate mice with 2.5% wt/vol DSS (molecular weight, 36,000–50,000 daltons; MP Biomedicals, Solon, OH) dissolved in sterile drinking water given ad libitum for 5 days, followed by 1 day of tap water.

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

    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