Structured Review

BioLegend mouse il 6
Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, <t>IL-6,</t> IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P
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Images

1) Product Images from "Human multipotent stromal cells attenuate lipopolysaccharide-induced acute lung injury in mice via secretion of tumor necrosis factor-?-induced protein 6"

Article Title: Human multipotent stromal cells attenuate lipopolysaccharide-induced acute lung injury in mice via secretion of tumor necrosis factor-?-induced protein 6

Journal: Stem Cell Research & Therapy

doi: 10.1186/scrt68

Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, IL-6, IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P
Figure Legend Snippet: Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, IL-6, IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P

Techniques Used: Expressing, Multiplex Assay

2) Product Images from "Loss of lung WWOX expression causes neutrophilic inflammation"

Article Title: Loss of lung WWOX expression causes neutrophilic inflammation

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

doi: 10.1152/ajplung.00034.2017

WWOX knockdown in human alveolar epithelial cells results in increased neutrophil chemotaxis. A549 cells grown in culture were transfected with control vs. WWOX-silencing miR-expressing plasmids. A : representative Western blot for WWOX in cell lysates. B and C : transfected A549 cells were grown in the bottom chamber of a Transwell plate containing 3-μm pores. Control IgG vs. neutralizing anti-IL-8 antibody was added to the media. Then, 1 × 10 5 human neutrophils were placed in the top chamber. Thirty minutes later, neutrophils were pelleted from the media in the bottom chamber and resuspended in a fixed volume, and a cytospin preparation was stained and examined under light microscopy. A representative image is shown here along with a scatter plot depicting the number of neutrophils counted per high-powered field. D–F : concentrations of IL-1β, IL-6, and IL-8 were measured by ELISA in the media supernatant of control vs. WWOX-silenced cells without anti-IL-8 neutralizing antibody or control IgG. Results are shown as means ± SD in n = 3 independent experiments. * P
Figure Legend Snippet: WWOX knockdown in human alveolar epithelial cells results in increased neutrophil chemotaxis. A549 cells grown in culture were transfected with control vs. WWOX-silencing miR-expressing plasmids. A : representative Western blot for WWOX in cell lysates. B and C : transfected A549 cells were grown in the bottom chamber of a Transwell plate containing 3-μm pores. Control IgG vs. neutralizing anti-IL-8 antibody was added to the media. Then, 1 × 10 5 human neutrophils were placed in the top chamber. Thirty minutes later, neutrophils were pelleted from the media in the bottom chamber and resuspended in a fixed volume, and a cytospin preparation was stained and examined under light microscopy. A representative image is shown here along with a scatter plot depicting the number of neutrophils counted per high-powered field. D–F : concentrations of IL-1β, IL-6, and IL-8 were measured by ELISA in the media supernatant of control vs. WWOX-silenced cells without anti-IL-8 neutralizing antibody or control IgG. Results are shown as means ± SD in n = 3 independent experiments. * P

Techniques Used: Chemotaxis Assay, Transfection, Expressing, Western Blot, Staining, Light Microscopy, Enzyme-linked Immunosorbent Assay

Pretreatment of mice with the JNK-inhibitor, SP600125, attenuates neutrophilic inflammation associated with loss of WWOX expression. Twelve C57Bl/6 mice were treated with intratracheal instillation of either control nontargeting ( n = 6) or WWOX-targeting siRNA ( n = 6). Three mice in each group were then administered the JNK inhibitor SP500125 (30 mg/kg) or an equivalent volume of DMSO subcutaneously. Bronchoalveolar lavage with 1 ml of PBS was performed. A–F : BAL neutrophil counts, protein concentration, and KC, MIP-2, IL-6, and IL-1β concentrations were measured. Results are shown as means ± SD in n = 3 independent experiments. * P
Figure Legend Snippet: Pretreatment of mice with the JNK-inhibitor, SP600125, attenuates neutrophilic inflammation associated with loss of WWOX expression. Twelve C57Bl/6 mice were treated with intratracheal instillation of either control nontargeting ( n = 6) or WWOX-targeting siRNA ( n = 6). Three mice in each group were then administered the JNK inhibitor SP500125 (30 mg/kg) or an equivalent volume of DMSO subcutaneously. Bronchoalveolar lavage with 1 ml of PBS was performed. A–F : BAL neutrophil counts, protein concentration, and KC, MIP-2, IL-6, and IL-1β concentrations were measured. Results are shown as means ± SD in n = 3 independent experiments. * P

Techniques Used: Mouse Assay, Expressing, Protein Concentration

Knockdown of WW domain-containing oxidoreductase (WWOX) expression in mouse lung causes neutrophil influx, vascular leak, and inflammatory cytokine production. Twelve C57Bl/6 mice were treated with intratracheal instillation of either control nontargeting ( n = 6) or WWOX-targeting siRNA ( n = 6). Seventy-two hours later 3 mice in each group received 40 µl of PBS via intratracheal instillation, and the remaining mice received 1 mg/kg LPS in a 40-µl volume. Eighteen hours later all mice underwent bronchoalveolar lavage (BAL) with 1 ml of PBS, followed by harvesting of the lungs for homogenization and Western blotting as well as histologic examination. A : representative Western blot for WWOX in mouse lung homogenates resolved by SDS-PAGE. B : representative hematoxylin-eosin-stained lung histologic sections from each of the 4 experimental conditions. BALF, bronchoalveolar lavage fluid. C–J : scatter plots depict BAL leukocyte counts, neutrophil counts, protein concentration, and FITC-dextran flux as a measure of permeability, and IL-1, IL-6, keratinocyte-derived chemokine (KC), and macrophage inhibitory-2 (MIP-2) concentrations, respectively. Results are shown as means ± SD in n = 3 independent experiments. A two-way ANOVA for PBS vs. LPS and control vs. WWOX siRNA was performed followed by a Student’s t -test for all significant comparisons. * P
Figure Legend Snippet: Knockdown of WW domain-containing oxidoreductase (WWOX) expression in mouse lung causes neutrophil influx, vascular leak, and inflammatory cytokine production. Twelve C57Bl/6 mice were treated with intratracheal instillation of either control nontargeting ( n = 6) or WWOX-targeting siRNA ( n = 6). Seventy-two hours later 3 mice in each group received 40 µl of PBS via intratracheal instillation, and the remaining mice received 1 mg/kg LPS in a 40-µl volume. Eighteen hours later all mice underwent bronchoalveolar lavage (BAL) with 1 ml of PBS, followed by harvesting of the lungs for homogenization and Western blotting as well as histologic examination. A : representative Western blot for WWOX in mouse lung homogenates resolved by SDS-PAGE. B : representative hematoxylin-eosin-stained lung histologic sections from each of the 4 experimental conditions. BALF, bronchoalveolar lavage fluid. C–J : scatter plots depict BAL leukocyte counts, neutrophil counts, protein concentration, and FITC-dextran flux as a measure of permeability, and IL-1, IL-6, keratinocyte-derived chemokine (KC), and macrophage inhibitory-2 (MIP-2) concentrations, respectively. Results are shown as means ± SD in n = 3 independent experiments. A two-way ANOVA for PBS vs. LPS and control vs. WWOX siRNA was performed followed by a Student’s t -test for all significant comparisons. * P

Techniques Used: Expressing, Mouse Assay, Homogenization, Western Blot, SDS Page, Staining, Protein Concentration, Permeability, Derivative Assay

Increased neutrophil chemotaxis in WWOX-silenced cells is dependent on IL-8 and c-Jun transcription factor activity. A549 cells grown in culture were transfected with either a single or dual WWOX- and c-Jun-silencing miR-expressing plasmid. A : representative Western blot for WWOX and c-Jun in cell lysates resolved by SDS-PAGE is shown. Note that since WWOX and c-Jun are of similar molecular weight, the bands for each are derived from separate gels that were run at the same time and that contained the same fractions of the same lysates. B : scatter plot illustrates the results of a neutrophil chemotaxis assay in n = 3 experiments. C–E : scatterplots depict measured concentrations of IL-8, IL-1β, and IL-6. F : results of an NF-kB assay on nuclear extracts. Results are shown as means ± SD in n = 3 independent experiments. * P
Figure Legend Snippet: Increased neutrophil chemotaxis in WWOX-silenced cells is dependent on IL-8 and c-Jun transcription factor activity. A549 cells grown in culture were transfected with either a single or dual WWOX- and c-Jun-silencing miR-expressing plasmid. A : representative Western blot for WWOX and c-Jun in cell lysates resolved by SDS-PAGE is shown. Note that since WWOX and c-Jun are of similar molecular weight, the bands for each are derived from separate gels that were run at the same time and that contained the same fractions of the same lysates. B : scatter plot illustrates the results of a neutrophil chemotaxis assay in n = 3 experiments. C–E : scatterplots depict measured concentrations of IL-8, IL-1β, and IL-6. F : results of an NF-kB assay on nuclear extracts. Results are shown as means ± SD in n = 3 independent experiments. * P

Techniques Used: Chemotaxis Assay, Activity Assay, Transfection, Expressing, Plasmid Preparation, Western Blot, SDS Page, Molecular Weight, Derivative Assay

3) Product Images from "Expression of adipocyte/macrophage fatty acid binding protein in tumor associated macrophages promotes breast cancer progression"

Article Title: Expression of adipocyte/macrophage fatty acid binding protein in tumor associated macrophages promotes breast cancer progression

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-17-2465

Expression of A-FABP in macrophages promotes IL-6 production
Figure Legend Snippet: Expression of A-FABP in macrophages promotes IL-6 production

Techniques Used: Expressing

A-FABP promotes IL-6 production via the NFκB/ miR-29b pathway in macrophages
Figure Legend Snippet: A-FABP promotes IL-6 production via the NFκB/ miR-29b pathway in macrophages

Techniques Used:

4) Product Images from "CD138 mediates selection of mature plasma cells by regulating their survival"

Article Title: CD138 mediates selection of mature plasma cells by regulating their survival

Journal: Blood

doi: 10.1182/blood-2017-01-761643

CD138 expression on ASCs promotes IL-6 signaling. (A-B,D) Mice were co-injected with purified transgenic B cells from WT and sdc1 −/− mice, immunized, and examined for YFP + ASCs on day 7. (A) dLN cells were briefly serum starved, incubated in the presence of recombinant IL-6 (rIL-6) for 20 minutes and analyzed for intracellular pSTAT3 by flow cytometry. Graph represents mean (± SEM) of YFP + pSTAT3 + cells. (B) Within the WT ASC compartment, mature CD138 + YFP + ASCs were distinguished from immature CD138 − YFP + ASCs by flow cytometry, and stained for pSTAT3 following ex vivo stimulation by rIL-6. Representative flow cytometry dot plots depict prior to (media) and after (+rIL6) rIL-6 stimulation (left). Graph represents mean (± SEM) of the percentage of YFP + pSTAT3 + cells from each subset (right). (C) Human PBMCs were examined by flow cytometry. Graph represents mean (± SEM) of the percentage of CD19 low CD38 high ASCs positive for pSTAT3 from within the CD138 + or CD138 − subsets following ex vivo stimulation by human rIL-6. (D) The dLN from immunized host mice were examined by flow cytometry. YFP + ASCs derived from either WT or sdc1-deficient B cells were examined for IL-6α receptor (CD126; left) or IL-6β (CD130; right) receptor expression. Graphs show mean of MFI from either WT (blue) or sdc1 −/− (red) cells. (E) dLN cells from immunized mice were briefly serum starved, incubated in the presence of rIL-6 or rIL-21 (10 ng/mL) for 20 minutes, and analyzed for intracellular pSTAT3 by flow cytometry. Graphs show mean (± SEM) of the percentage of YFP + cells stained for pSTAT3. (F) Purified B cells from WT and CD138-deficient mice (sdc1 −/− ) were cocultured with LPS to generate ASCs in vitro. On day 3, cells were incubated in media in the presence (fresh) or absence (serum starved) of fetal calf serum, and stimulated with rIL-6 (either 1, 5, or 10 ng/mL). pSTAT3 levels were examined by flow cytometry. Graph depicts mean (± SEM) of the percentage of YFP + pSTAT3 + cells. (G) In vivo generated YFP + ASCs were stained with 10E4 antibody to detect HS. Heparinase III-treated cells that lack HS surface expression is used as a control. Graph represents the MFI of 10E4 expression on various subsets relative to heparinase III-treated cells. * P
Figure Legend Snippet: CD138 expression on ASCs promotes IL-6 signaling. (A-B,D) Mice were co-injected with purified transgenic B cells from WT and sdc1 −/− mice, immunized, and examined for YFP + ASCs on day 7. (A) dLN cells were briefly serum starved, incubated in the presence of recombinant IL-6 (rIL-6) for 20 minutes and analyzed for intracellular pSTAT3 by flow cytometry. Graph represents mean (± SEM) of YFP + pSTAT3 + cells. (B) Within the WT ASC compartment, mature CD138 + YFP + ASCs were distinguished from immature CD138 − YFP + ASCs by flow cytometry, and stained for pSTAT3 following ex vivo stimulation by rIL-6. Representative flow cytometry dot plots depict prior to (media) and after (+rIL6) rIL-6 stimulation (left). Graph represents mean (± SEM) of the percentage of YFP + pSTAT3 + cells from each subset (right). (C) Human PBMCs were examined by flow cytometry. Graph represents mean (± SEM) of the percentage of CD19 low CD38 high ASCs positive for pSTAT3 from within the CD138 + or CD138 − subsets following ex vivo stimulation by human rIL-6. (D) The dLN from immunized host mice were examined by flow cytometry. YFP + ASCs derived from either WT or sdc1-deficient B cells were examined for IL-6α receptor (CD126; left) or IL-6β (CD130; right) receptor expression. Graphs show mean of MFI from either WT (blue) or sdc1 −/− (red) cells. (E) dLN cells from immunized mice were briefly serum starved, incubated in the presence of rIL-6 or rIL-21 (10 ng/mL) for 20 minutes, and analyzed for intracellular pSTAT3 by flow cytometry. Graphs show mean (± SEM) of the percentage of YFP + cells stained for pSTAT3. (F) Purified B cells from WT and CD138-deficient mice (sdc1 −/− ) were cocultured with LPS to generate ASCs in vitro. On day 3, cells were incubated in media in the presence (fresh) or absence (serum starved) of fetal calf serum, and stimulated with rIL-6 (either 1, 5, or 10 ng/mL). pSTAT3 levels were examined by flow cytometry. Graph depicts mean (± SEM) of the percentage of YFP + pSTAT3 + cells. (G) In vivo generated YFP + ASCs were stained with 10E4 antibody to detect HS. Heparinase III-treated cells that lack HS surface expression is used as a control. Graph represents the MFI of 10E4 expression on various subsets relative to heparinase III-treated cells. * P

Techniques Used: Expressing, Mouse Assay, Injection, Purification, Transgenic Assay, Incubation, Recombinant, Flow Cytometry, Cytometry, Staining, Ex Vivo, Derivative Assay, In Vitro, In Vivo, Generated

5) Product Images from "Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485"

Article Title: Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485

Journal: Immune Network

doi: 10.4110/in.2018.18.e18

Effects of MHY1485 on FcεRI-mediated degranulation and cytokine production in mast cells. BMMCs were sensitized for 5 h, incubated with the indicated concentration of MHY1485 for 1 h, and then either unstimulated (unstim) or stimulated with the DNP-HSA Ag. (A) Time-course immunoblot analysis for mTOR signaling, with or without MHY1485, following Ag stimulation. Band densities of pS6K on Thr389 and pAkt on Ser473 were normalized to their total protein expression from the results of 3 independent experiments. AU represents arbitrary unit. (B) Degranulation was assessed by measuring β-hexosaminidase release 30 min after stimulation. (C) The levels of IL-6 and TNF-α proteins in the media were analyzed using ELISA 6 h after stimulation. (D) qRT-PCR analysis for FcεRI-mediated induction of Il6 and Tfna mRNA was carried out 1 h after Ag stimulation. Bar graphs are shown as mean±standard error of the mean of triplicates and are representative of 3 independent experiments. A p-value of less than 0.05 between stimulated groups with and without MHY1485 treatment is judged significant and indicated. pS6K, phospho-S6K; Thr389, threonine 389; pAkt, phospho-Akt; Ser473, serine 473; qRT-PCR, quantitative real-time PCR. * p
Figure Legend Snippet: Effects of MHY1485 on FcεRI-mediated degranulation and cytokine production in mast cells. BMMCs were sensitized for 5 h, incubated with the indicated concentration of MHY1485 for 1 h, and then either unstimulated (unstim) or stimulated with the DNP-HSA Ag. (A) Time-course immunoblot analysis for mTOR signaling, with or without MHY1485, following Ag stimulation. Band densities of pS6K on Thr389 and pAkt on Ser473 were normalized to their total protein expression from the results of 3 independent experiments. AU represents arbitrary unit. (B) Degranulation was assessed by measuring β-hexosaminidase release 30 min after stimulation. (C) The levels of IL-6 and TNF-α proteins in the media were analyzed using ELISA 6 h after stimulation. (D) qRT-PCR analysis for FcεRI-mediated induction of Il6 and Tfna mRNA was carried out 1 h after Ag stimulation. Bar graphs are shown as mean±standard error of the mean of triplicates and are representative of 3 independent experiments. A p-value of less than 0.05 between stimulated groups with and without MHY1485 treatment is judged significant and indicated. pS6K, phospho-S6K; Thr389, threonine 389; pAkt, phospho-Akt; Ser473, serine 473; qRT-PCR, quantitative real-time PCR. * p

Techniques Used: Incubation, Concentration Assay, Expressing, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

6) Product Images from "Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485"

Article Title: Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485

Journal: Immune Network

doi: 10.4110/in.2018.18.e18

Effects of MHY1485 on FcεRI-mediated degranulation and cytokine production in mast cells. BMMCs were sensitized for 5 h, incubated with the indicated concentration of MHY1485 for 1 h, and then either unstimulated (unstim) or stimulated with the DNP-HSA Ag. (A) Time-course immunoblot analysis for mTOR signaling, with or without MHY1485, following Ag stimulation. Band densities of pS6K on Thr389 and pAkt on Ser473 were normalized to their total protein expression from the results of 3 independent experiments. AU represents arbitrary unit. (B) Degranulation was assessed by measuring β-hexosaminidase release 30 min after stimulation. (C) The levels of IL-6 and TNF-α proteins in the media were analyzed using ELISA 6 h after stimulation. (D) qRT-PCR analysis for FcεRI-mediated induction of Il6 and Tfna mRNA was carried out 1 h after Ag stimulation. Bar graphs are shown as mean±standard error of the mean of triplicates and are representative of 3 independent experiments. A p-value of less than 0.05 between stimulated groups with and without MHY1485 treatment is judged significant and indicated. pS6K, phospho-S6K; Thr389, threonine 389; pAkt, phospho-Akt; Ser473, serine 473; qRT-PCR, quantitative real-time PCR. * p
Figure Legend Snippet: Effects of MHY1485 on FcεRI-mediated degranulation and cytokine production in mast cells. BMMCs were sensitized for 5 h, incubated with the indicated concentration of MHY1485 for 1 h, and then either unstimulated (unstim) or stimulated with the DNP-HSA Ag. (A) Time-course immunoblot analysis for mTOR signaling, with or without MHY1485, following Ag stimulation. Band densities of pS6K on Thr389 and pAkt on Ser473 were normalized to their total protein expression from the results of 3 independent experiments. AU represents arbitrary unit. (B) Degranulation was assessed by measuring β-hexosaminidase release 30 min after stimulation. (C) The levels of IL-6 and TNF-α proteins in the media were analyzed using ELISA 6 h after stimulation. (D) qRT-PCR analysis for FcεRI-mediated induction of Il6 and Tfna mRNA was carried out 1 h after Ag stimulation. Bar graphs are shown as mean±standard error of the mean of triplicates and are representative of 3 independent experiments. A p-value of less than 0.05 between stimulated groups with and without MHY1485 treatment is judged significant and indicated. pS6K, phospho-S6K; Thr389, threonine 389; pAkt, phospho-Akt; Ser473, serine 473; qRT-PCR, quantitative real-time PCR. * p

Techniques Used: Incubation, Concentration Assay, Expressing, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

7) Product Images from "A Novel Hepatic Anti-Fibrotic Strategy Utilizing the Secretome Released from Etanercept-Synthesizing Adipose-Derived Stem Cells"

Article Title: A Novel Hepatic Anti-Fibrotic Strategy Utilizing the Secretome Released from Etanercept-Synthesizing Adipose-Derived Stem Cells

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms20246302

Anti-fibrotic effects of the etanercept-secretome in an in vivo model of liver fibrosis. ( A ) Effects of etanercept-secretome on the serum levels of liver enzymes. Of mice with two kinds of secretome treatment (control secretome and etanercept-secretome), etanercept-secretome group showed the significantly lower AST and ALT than did control secretome group. ( B ) Effects of etanercept-secretome on the serum levels of pro-inflammatory cytokines (TNF-α and IL-6). Etanercept-secretome group showed the lowest serum levels of TNF-α and IL-6 of all. The values are presented as mean ± standard deviation of three independent experiments. Abbreviations: ALT, alanine transaminase; AST, aspartate transaminase; COL1A1, collagen type 1 alpha1; CS, secretome obtained from empty vector-transfected ASCs; Ct, control; ES, etanercept-secretome (secretome obtained from etanercept-synthesizing ASCs); Sal, saline injection group; TNF-α, tumor necrosis factor-α.
Figure Legend Snippet: Anti-fibrotic effects of the etanercept-secretome in an in vivo model of liver fibrosis. ( A ) Effects of etanercept-secretome on the serum levels of liver enzymes. Of mice with two kinds of secretome treatment (control secretome and etanercept-secretome), etanercept-secretome group showed the significantly lower AST and ALT than did control secretome group. ( B ) Effects of etanercept-secretome on the serum levels of pro-inflammatory cytokines (TNF-α and IL-6). Etanercept-secretome group showed the lowest serum levels of TNF-α and IL-6 of all. The values are presented as mean ± standard deviation of three independent experiments. Abbreviations: ALT, alanine transaminase; AST, aspartate transaminase; COL1A1, collagen type 1 alpha1; CS, secretome obtained from empty vector-transfected ASCs; Ct, control; ES, etanercept-secretome (secretome obtained from etanercept-synthesizing ASCs); Sal, saline injection group; TNF-α, tumor necrosis factor-α.

Techniques Used: In Vivo, Mouse Assay, AST Assay, Standard Deviation, Plasmid Preparation, Transfection, Injection

8) Product Images from "The kinases Mst1 and Mst2 positively regulate phagocyte ROS induction and bactericidal activity"

Article Title: The kinases Mst1 and Mst2 positively regulate phagocyte ROS induction and bactericidal activity

Journal: Nature immunology

doi: 10.1038/ni.3268

Losses of Mst1 and Mst2 increase susceptibility to bacterial sepsis ( a ) Representative lung tissues and H E staining of lung sections from wild type and Mst1 −/− Mst2 fl/fl Vav- Cre mice. Scale bar, 100 μm. ( b-e ) Mst1 fl/fl Mst2 fl/fl (WT) or Mst1 fl/fl Mst2 fl/fl Lyz2- Cre (cDKO) mice (n=10 mice per group per experiment) subjected to sublethal CLP; mortality (Mantel–Cox test)( b ), serum cytokines measured by ELISAs ( c ), inflammatory cell infiltration in the lungs as shown by H E staining ( d ) and the bacterial loads (colony forming units, CFU) measured in the lung, liver, spleen, kidney and peritoneal fluid ( e ) after CLP induction. Scale bar, 50 μm. ( f ) Immunoblot analysis of P-p38, P-Jnk, IκBα and P-Mob1 in WT BMDMs stimulated with indicated TLR agonists for different durations. ( g ) Immunoblot analysis of P-Mob1 and MyD88 in WT or MyD88 KO RAW246.7 cells stimulated with the indicated agonists for different durations. ( h ) WT or cDKO BMDMs were stimulated with LPS for the indicated times, followed by immunoblot analysis with the indicated antibodies. ( i ) WT and cDKO BMDMs or neutrophils were treated with LPS (100 ng/ml) for the indicated times. Cytokine (IL-6 and TNF) production was measured by ELISA. Data were assessed with Student's t -test and are presented as mean ± s.d. ns, no significant, * p
Figure Legend Snippet: Losses of Mst1 and Mst2 increase susceptibility to bacterial sepsis ( a ) Representative lung tissues and H E staining of lung sections from wild type and Mst1 −/− Mst2 fl/fl Vav- Cre mice. Scale bar, 100 μm. ( b-e ) Mst1 fl/fl Mst2 fl/fl (WT) or Mst1 fl/fl Mst2 fl/fl Lyz2- Cre (cDKO) mice (n=10 mice per group per experiment) subjected to sublethal CLP; mortality (Mantel–Cox test)( b ), serum cytokines measured by ELISAs ( c ), inflammatory cell infiltration in the lungs as shown by H E staining ( d ) and the bacterial loads (colony forming units, CFU) measured in the lung, liver, spleen, kidney and peritoneal fluid ( e ) after CLP induction. Scale bar, 50 μm. ( f ) Immunoblot analysis of P-p38, P-Jnk, IκBα and P-Mob1 in WT BMDMs stimulated with indicated TLR agonists for different durations. ( g ) Immunoblot analysis of P-Mob1 and MyD88 in WT or MyD88 KO RAW246.7 cells stimulated with the indicated agonists for different durations. ( h ) WT or cDKO BMDMs were stimulated with LPS for the indicated times, followed by immunoblot analysis with the indicated antibodies. ( i ) WT and cDKO BMDMs or neutrophils were treated with LPS (100 ng/ml) for the indicated times. Cytokine (IL-6 and TNF) production was measured by ELISA. Data were assessed with Student's t -test and are presented as mean ± s.d. ns, no significant, * p

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

9) Product Images from "Mycolactone displays anti-inflammatory effects on the nervous system"

Article Title: Mycolactone displays anti-inflammatory effects on the nervous system

Journal: PLoS Neglected Tropical Diseases

doi: 10.1371/journal.pntd.0006058

Mycolactone suppresses the production of pro-inflammatory mediators by activated microglia. IL-6 (A) and TNF-α (B) production by primary mouse cortical microglia exposed to mycolactone (ML) or vehicle for 16 h, prior to a 8 h activation with 100 ng/ml LPS. (C) Flow cytometry analysis of intracellular NOS-2 in primary cortical microglia pre-treated with ML for 30 min, prior to 16 h activation with 100 ng/ml LPS + 20 ng/ml IFN-γ, in presence of ML. (D) Flow cytometry analysis of surface expression of TLR4 (black) and IFN-γ receptor (CD119, gray) in microglia exposed to ML for 16 h. Data are means IL-6 or TNF-α levels ± SEM (A-B), mean fluorescence intensity ± SEM (C) and mean percentage of suppression compared to vehicle (D) of duplicates, and are representative of two independent experiments.
Figure Legend Snippet: Mycolactone suppresses the production of pro-inflammatory mediators by activated microglia. IL-6 (A) and TNF-α (B) production by primary mouse cortical microglia exposed to mycolactone (ML) or vehicle for 16 h, prior to a 8 h activation with 100 ng/ml LPS. (C) Flow cytometry analysis of intracellular NOS-2 in primary cortical microglia pre-treated with ML for 30 min, prior to 16 h activation with 100 ng/ml LPS + 20 ng/ml IFN-γ, in presence of ML. (D) Flow cytometry analysis of surface expression of TLR4 (black) and IFN-γ receptor (CD119, gray) in microglia exposed to ML for 16 h. Data are means IL-6 or TNF-α levels ± SEM (A-B), mean fluorescence intensity ± SEM (C) and mean percentage of suppression compared to vehicle (D) of duplicates, and are representative of two independent experiments.

Techniques Used: Activation Assay, Flow Cytometry, Cytometry, Expressing, Fluorescence

Intrathecal injection of mycolactone triggers a decrease of pro-inflammatory cytokines in spinal cord of Sham rats. (A) Experimental procedure: chronic constriction injury (CCI) was induced in rats by partial ligation of the sciatic nerve. At day 2 (D2) post-operation, rats were treated daily by intrathecal injections of mycolactone (ML) or vehicle (Veh) during 3 days and were sacrificed at D5. Sham-operated rats were submitted to the same procedure without CCI. Ipsilateral DRGs from lumbar regions 4 to 6 (L4-L6) and ipsilateral dorsal horn of the spinal cord were collected. (B-G) Expression levels of the pro-inflammatory mediators Il-1β, TIMP-1, IL-6, IFN-γ and IL-2 in the spinal cord (SpC) or in the dorsal root ganglion (DRG), 5 days post CCI or Sham treatment, in Vehicle or ML injected rats. Mean fold changes ± SEM compared to sham treated rats injected with vehicle (n = 6–9). Statistics: Mann whitney, * p
Figure Legend Snippet: Intrathecal injection of mycolactone triggers a decrease of pro-inflammatory cytokines in spinal cord of Sham rats. (A) Experimental procedure: chronic constriction injury (CCI) was induced in rats by partial ligation of the sciatic nerve. At day 2 (D2) post-operation, rats were treated daily by intrathecal injections of mycolactone (ML) or vehicle (Veh) during 3 days and were sacrificed at D5. Sham-operated rats were submitted to the same procedure without CCI. Ipsilateral DRGs from lumbar regions 4 to 6 (L4-L6) and ipsilateral dorsal horn of the spinal cord were collected. (B-G) Expression levels of the pro-inflammatory mediators Il-1β, TIMP-1, IL-6, IFN-γ and IL-2 in the spinal cord (SpC) or in the dorsal root ganglion (DRG), 5 days post CCI or Sham treatment, in Vehicle or ML injected rats. Mean fold changes ± SEM compared to sham treated rats injected with vehicle (n = 6–9). Statistics: Mann whitney, * p

Techniques Used: Injection, Ligation, Expressing, MANN-WHITNEY

Anti-inflammatory effects of mycolactone on primary DRG and Schwann cells. Production of CCL-2 (A), IL-6 (B) and TNF-α (C) by mouse dorsal root ganglion (DRG) cells exposed to subtoxic doses of mycolactone (ML) or equivalent volume of vehicle (DMSO) for 30 min prior to 16 h of stimulation with 1 μg/ml LPS. Controls (NA) are vehicle-treated, non-activated cells. (D) IL-6 production by Schwann cells (SCs) exposed to ML or vehicle (DMSO) for 30 min prior to stimulation with 1 μg/m LPS + 20 ng/ml IFN-γ or not (NA). (E) Flow cytometry analysis of TLR4 surface expression by SCs exposed to increasing doses of ML for 16 h. Data are mean values of OD or MFI ± SEM of triplicates, and are representative of two independent experiments.
Figure Legend Snippet: Anti-inflammatory effects of mycolactone on primary DRG and Schwann cells. Production of CCL-2 (A), IL-6 (B) and TNF-α (C) by mouse dorsal root ganglion (DRG) cells exposed to subtoxic doses of mycolactone (ML) or equivalent volume of vehicle (DMSO) for 30 min prior to 16 h of stimulation with 1 μg/ml LPS. Controls (NA) are vehicle-treated, non-activated cells. (D) IL-6 production by Schwann cells (SCs) exposed to ML or vehicle (DMSO) for 30 min prior to stimulation with 1 μg/m LPS + 20 ng/ml IFN-γ or not (NA). (E) Flow cytometry analysis of TLR4 surface expression by SCs exposed to increasing doses of ML for 16 h. Data are mean values of OD or MFI ± SEM of triplicates, and are representative of two independent experiments.

Techniques Used: Flow Cytometry, Cytometry, Expressing

10) Product Images from "SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction"

Article Title: SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction

Journal: PLoS ONE

doi: 10.1371/journal.pone.0072492

Effects of restoring SR-BI expression in BM derived cells on plasma levels of TNFα and IL-6 in HFCC diet fed SR-BI-null/apoE-hypomorphic mice. A. TNFα and B. IL-6 levels in plasma from control SR-BI −/− → SR-BI −/− (white bars) and SR-BI +/+ → SR-BI −/− mice (black bars) after 3 weeks of HFCC diet feeding. Shown are mean levels for n = 8 mice per group. Error bars correspond to standard errors. A. TNFα levels were not statistically significantly different. B. IL-6 levels were statistically significantly different. P = 0.028. Statistical analysis was by the Mann-Whitney rank sum test.
Figure Legend Snippet: Effects of restoring SR-BI expression in BM derived cells on plasma levels of TNFα and IL-6 in HFCC diet fed SR-BI-null/apoE-hypomorphic mice. A. TNFα and B. IL-6 levels in plasma from control SR-BI −/− → SR-BI −/− (white bars) and SR-BI +/+ → SR-BI −/− mice (black bars) after 3 weeks of HFCC diet feeding. Shown are mean levels for n = 8 mice per group. Error bars correspond to standard errors. A. TNFα levels were not statistically significantly different. B. IL-6 levels were statistically significantly different. P = 0.028. Statistical analysis was by the Mann-Whitney rank sum test.

Techniques Used: Expressing, Derivative Assay, Mouse Assay, MANN-WHITNEY

11) Product Images from "The Complement Anaphylatoxins, C5a and C3a, Suppress Interferon-Beta Production in Response to Listeria monocytogenes by Inhibition of the Cyclic Dinucleotide-Activated Cytosolic Surveillance Pathway"

Article Title: The Complement Anaphylatoxins, C5a and C3a, Suppress Interferon-Beta Production in Response to Listeria monocytogenes by Inhibition of the Cyclic Dinucleotide-Activated Cytosolic Surveillance Pathway

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

doi: 10.4049/jimmunol.1601420

C5a and C3a suppress IFN-β production in BMDCs WT BMDCs were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h, and then the cells were infected with Lm overnight. Cell-free supernatants were used to quantitate (A) IFN-β production or (B) IL-6, TNF-α, and MCP-1 production. (C) WT BMDCs were pre-treated with either media, 50 nM C5a, 100 nM C5aA, 500 nM C3a, or 100 nM C3aA for 2 h and then were incubated with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. (D) C5aR−/− BMDCs were pre-treated with either media, 50 nM C5a, or 100 nM C5aA for 2 h and (E) C3aR−/− BMDCs were pre-treated with either media, 500 nM C3a, or 100 nM C3aA for 2 h, and then the cells were incubated with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P ≤ 0.017; ** P ≤ 0.009; *** P = 0.0006 by t test.
Figure Legend Snippet: C5a and C3a suppress IFN-β production in BMDCs WT BMDCs were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h, and then the cells were infected with Lm overnight. Cell-free supernatants were used to quantitate (A) IFN-β production or (B) IL-6, TNF-α, and MCP-1 production. (C) WT BMDCs were pre-treated with either media, 50 nM C5a, 100 nM C5aA, 500 nM C3a, or 100 nM C3aA for 2 h and then were incubated with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. (D) C5aR−/− BMDCs were pre-treated with either media, 50 nM C5a, or 100 nM C5aA for 2 h and (E) C3aR−/− BMDCs were pre-treated with either media, 500 nM C3a, or 100 nM C3aA for 2 h, and then the cells were incubated with 25 μg/ml c-di-AMP for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P ≤ 0.017; ** P ≤ 0.009; *** P = 0.0006 by t test.

Techniques Used: Infection, Incubation

C5a and C3a suppress IFN-β production in J774A.1 cells J774A.1 cells were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h and then the cells were infected with Lm for 20 h. Cell-free supernatants were used to quantitate (A) IFN-β production or (B) IL-6, TNF-α, and MCP-1 production. J774A.1 cells were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h and then were incubated with (C) 25 μg/ml c-di-AMP or (D) 100 ng/ml LPS for 20 h. IFN-β was quantitated from cell-free supernatants. (E) J774A.1 cells were pre-treated with either media or 50 nM C5a for 30 min, 1 h, 2 h, 4 h, or 8 h and then were incubated with 100 ng/ml LPS for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P = 0.027; ** P ≤ 0.006; *** P ≤ 0.0001 by t test.
Figure Legend Snippet: C5a and C3a suppress IFN-β production in J774A.1 cells J774A.1 cells were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h and then the cells were infected with Lm for 20 h. Cell-free supernatants were used to quantitate (A) IFN-β production or (B) IL-6, TNF-α, and MCP-1 production. J774A.1 cells were pre-treated with either media, 50 nM C5a, or 500 nM C3a for 2 h and then were incubated with (C) 25 μg/ml c-di-AMP or (D) 100 ng/ml LPS for 20 h. IFN-β was quantitated from cell-free supernatants. (E) J774A.1 cells were pre-treated with either media or 50 nM C5a for 30 min, 1 h, 2 h, 4 h, or 8 h and then were incubated with 100 ng/ml LPS for 20 h. IFN-β was quantitated from cell-free supernatants. All data are presented as mean pg/ml ± SEM. These data are pooled from three independent experiments. * P = 0.027; ** P ≤ 0.006; *** P ≤ 0.0001 by t test.

Techniques Used: Infection, Incubation

12) Product Images from "Ablation of XP-V gene causes adipose tissue senescence and metabolic abnormalities"

Article Title: Ablation of XP-V gene causes adipose tissue senescence and metabolic abnormalities

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

doi: 10.1073/pnas.1506954112

Real-time PCR analysis of relative mRNA expression in mouse adipocytes. ( A ) Relative mRNA expression of IL-6, TNF-α, MCP-1, and adiponectin in mouse adipocytes. ( B ) Real-time PCR analysis of relative mRNA expression of PPAR-γ and SREBP1 in mouse adipocytes. The data, which are shown as the mean ± SEM ( n = 6), were analyzed by the Student t test (* P
Figure Legend Snippet: Real-time PCR analysis of relative mRNA expression in mouse adipocytes. ( A ) Relative mRNA expression of IL-6, TNF-α, MCP-1, and adiponectin in mouse adipocytes. ( B ) Real-time PCR analysis of relative mRNA expression of PPAR-γ and SREBP1 in mouse adipocytes. The data, which are shown as the mean ± SEM ( n = 6), were analyzed by the Student t test (* P

Techniques Used: Real-time Polymerase Chain Reaction, Expressing

NAC and Met suppressed DNA damage and metabolic abnormalities in pol η −/− mice fed high-fat diets. ( A ) Immunohistochemistry of 8-oxoG (arrows) in adipose specimens from WT and pol η −/− mice fed an HF diet. (Scale bars: 100 μM.) ( B ) Quantitation of alkaline comet assay of the adipocytes obtained from mice fed an HF diet with NAC or Met for 20 wk ( n = 200) or normal chow for 72 wk. ( C ) Body weight gain for mice fed a regular chow or HF diet with or without NAC. Body fat ( D ), plasma insulin ( E ), glucose intolerance ( F ), and plasma IL-6 level ( G ) are shown. The data, which are shown as the mean ± SEM ( n = 10), were analyzed by one-way ANOVA ( *P
Figure Legend Snippet: NAC and Met suppressed DNA damage and metabolic abnormalities in pol η −/− mice fed high-fat diets. ( A ) Immunohistochemistry of 8-oxoG (arrows) in adipose specimens from WT and pol η −/− mice fed an HF diet. (Scale bars: 100 μM.) ( B ) Quantitation of alkaline comet assay of the adipocytes obtained from mice fed an HF diet with NAC or Met for 20 wk ( n = 200) or normal chow for 72 wk. ( C ) Body weight gain for mice fed a regular chow or HF diet with or without NAC. Body fat ( D ), plasma insulin ( E ), glucose intolerance ( F ), and plasma IL-6 level ( G ) are shown. The data, which are shown as the mean ± SEM ( n = 10), were analyzed by one-way ANOVA ( *P

Techniques Used: Mouse Assay, Immunohistochemistry, Quantitation Assay, Alkaline Single Cell Gel Electrophoresis

NAC and Met suppressed DNA damage and metabolic abnormalities in pol η −/− mice. ( A ) mRNA expression of ATM, p53, p21, NF-κB, IL-6, TNF-α, and MCP-1 in the adipocytes of 4- and 72-wk-old mice treated with NAC or Met. ( B ) Drinking water uptake of WT and Pol η −/− mice fed a regular chow diet with or without NAC. NAC and Met suppressed body weight gain ( C and D ), body fat ( E ), plasma insulin ( F ), hypertrophy and hepatic steatosis ( G ), and glucose intolerance ( H ) ( n = 10). Ctl, control. The data, which are shown as the mean ± SEM, were analyzed by one-way ANOVA ( *P
Figure Legend Snippet: NAC and Met suppressed DNA damage and metabolic abnormalities in pol η −/− mice. ( A ) mRNA expression of ATM, p53, p21, NF-κB, IL-6, TNF-α, and MCP-1 in the adipocytes of 4- and 72-wk-old mice treated with NAC or Met. ( B ) Drinking water uptake of WT and Pol η −/− mice fed a regular chow diet with or without NAC. NAC and Met suppressed body weight gain ( C and D ), body fat ( E ), plasma insulin ( F ), hypertrophy and hepatic steatosis ( G ), and glucose intolerance ( H ) ( n = 10). Ctl, control. The data, which are shown as the mean ± SEM, were analyzed by one-way ANOVA ( *P

Techniques Used: Mouse Assay, Expressing, CTL Assay

Pol η −/− mice develop metabolic abnormalities. ( A ) Autopsy of WT and pol η −/− mice at 4 (4W) and 72 (72W) wk of age; ( B ) body weight gain ( n = 12); ( C ) body fat percentages ( n = 12); ( D ) circulating leptin and ( E ) insulin levels; ( F ) HOMA-IR ( n = 8); ( G ) glucose tolerance test (GTT) with area under curve (AUC) ( n = 8); ( H ) liver stained with Oil Red O (Scale bars: 50 μM); ( I ) H E staining of adipose macrophage infiltration; ( J ) F4/80 + /CD11b + -positive cells ( n = 6) in adipocytes from mice at 72 wk (w) of age; ( K ) IL-6; ( L ) TNF-α; ( M ) adiponectin in plasma ( n = 8); ( N ) H E staining of visceral fat histological sections; ( O ) quantitation of adipocyte size ( n = 400); and ( P ) expression of PPAR-γ, SREBP1-p125, and SREBP1-p68 subunits. Histological pictures and blots are representative of six independent experiments. The graphical data, which are shown as the mean ± SEM, were analyzed by the Student t test (* P
Figure Legend Snippet: Pol η −/− mice develop metabolic abnormalities. ( A ) Autopsy of WT and pol η −/− mice at 4 (4W) and 72 (72W) wk of age; ( B ) body weight gain ( n = 12); ( C ) body fat percentages ( n = 12); ( D ) circulating leptin and ( E ) insulin levels; ( F ) HOMA-IR ( n = 8); ( G ) glucose tolerance test (GTT) with area under curve (AUC) ( n = 8); ( H ) liver stained with Oil Red O (Scale bars: 50 μM); ( I ) H E staining of adipose macrophage infiltration; ( J ) F4/80 + /CD11b + -positive cells ( n = 6) in adipocytes from mice at 72 wk (w) of age; ( K ) IL-6; ( L ) TNF-α; ( M ) adiponectin in plasma ( n = 8); ( N ) H E staining of visceral fat histological sections; ( O ) quantitation of adipocyte size ( n = 400); and ( P ) expression of PPAR-γ, SREBP1-p125, and SREBP1-p68 subunits. Histological pictures and blots are representative of six independent experiments. The graphical data, which are shown as the mean ± SEM, were analyzed by the Student t test (* P

Techniques Used: Mouse Assay, Staining, Quantitation Assay, Expressing

Correlation between pol η expression, DNA damage, cell senescence, and lipid accumulation in 3T3L1 and MEF cell systems. ( A – D ) 3T3L1cells. ( A ) Quantitation of expression and activation of DNA damage, senescence, and adipogenic protein markers. ( B ) IL-6 secretion. ( C ) SA–β-gal activity. ( D ) Oil Red O staining ( n = 6). ( E – H ) MEF cells. ( E ) Quantitation of expression and activation of DNA damage, senescence, and adipogenic protein markers in WT, pol η −/− , pol η −/− -hPol η WT, and pol η −/− -hPol η R61F MEF cells. ( F ) IL-6 secretion ( n = 6). ( G ) SA–β-gal activity. ( H ) Oil Red O staining. The images presented were in the same scale. The graphical data are shown as the mean ± SEM. The data were analyzed by the Student t test (* P
Figure Legend Snippet: Correlation between pol η expression, DNA damage, cell senescence, and lipid accumulation in 3T3L1 and MEF cell systems. ( A – D ) 3T3L1cells. ( A ) Quantitation of expression and activation of DNA damage, senescence, and adipogenic protein markers. ( B ) IL-6 secretion. ( C ) SA–β-gal activity. ( D ) Oil Red O staining ( n = 6). ( E – H ) MEF cells. ( E ) Quantitation of expression and activation of DNA damage, senescence, and adipogenic protein markers in WT, pol η −/− , pol η −/− -hPol η WT, and pol η −/− -hPol η R61F MEF cells. ( F ) IL-6 secretion ( n = 6). ( G ) SA–β-gal activity. ( H ) Oil Red O staining. The images presented were in the same scale. The graphical data are shown as the mean ± SEM. The data were analyzed by the Student t test (* P

Techniques Used: Expressing, Quantitation Assay, Activation Assay, Activity Assay, Staining

Cellular senescence in adipose tissues and metabolic abnormalities. ( A and B ) SA–β-gal activity and quantitation from WT or pol η −/− mice at different ages ( n = 8). (Scale bar: 1 cm.) ( C and D ) Expression of senescent and apoptotic proteins and quantitation ( n = 6). PFT-α suppressed adipose senescence and metabolic abnormalities. ( E and F ) SA–β-gal activity ( Top ) and Oil Red O staining ( Bottom ) of SVF (mainly preadipocytes) and mature adipocytes through the differentiation process. (Scale bars: 200 μM.) SA–β-gal activity and quantitation ( n = 6) ( G and H ), IL-6 ( I ), body weight gain ( J ), body fat ( K ), plasma insulin ( L ), and GTT analysis ( n = 6) ( M ) are shown. C, control; HF, high fat; P, PFT-α.The graphical data were shown as the mean ± SEM. The data were analyzed by one-way ANOVA (* P
Figure Legend Snippet: Cellular senescence in adipose tissues and metabolic abnormalities. ( A and B ) SA–β-gal activity and quantitation from WT or pol η −/− mice at different ages ( n = 8). (Scale bar: 1 cm.) ( C and D ) Expression of senescent and apoptotic proteins and quantitation ( n = 6). PFT-α suppressed adipose senescence and metabolic abnormalities. ( E and F ) SA–β-gal activity ( Top ) and Oil Red O staining ( Bottom ) of SVF (mainly preadipocytes) and mature adipocytes through the differentiation process. (Scale bars: 200 μM.) SA–β-gal activity and quantitation ( n = 6) ( G and H ), IL-6 ( I ), body weight gain ( J ), body fat ( K ), plasma insulin ( L ), and GTT analysis ( n = 6) ( M ) are shown. C, control; HF, high fat; P, PFT-α.The graphical data were shown as the mean ± SEM. The data were analyzed by one-way ANOVA (* P

Techniques Used: Activity Assay, Quantitation Assay, Mouse Assay, Expressing, Staining

13) Product Images from "Stearic acid induces CD11c expression in proinflammatory macrophages via epidermal fatty acid binding protein"

Article Title: Stearic acid induces CD11c expression in proinflammatory macrophages via epidermal fatty acid binding protein

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

doi: 10.4049/jimmunol.1701416

E-FABP deficiency protects high saturated fat-induced skin lesions (A) Weight of WT mice and E-FABP−/− mice before and after cocoa butter diet (45% fat) (n=16 for WT mice, and n=15/E-FABP−/− mice) and safflower diet (45% fat) (n=10/WT mice and n=15/E-FABP−/−) for 6 months. ( B ) The incidence of skin lesions in WT and E-FABP−/− mice fed with cocoa butter diet or safflower oil diet for 9 months. (C-D) Confocal analysis of CD11c+ macrophage infiltration (green color) in the skin tissue of WT and E-FABP−/− mice fed with cocoa butter for 9 months. Relative CD11c fluorescent intensity is shown in panel D . (E-G) Flow cytometric analysis of CD80 ( E ), CD86 ( F ) and MHCII ( G ) expression on CD11c+ macrophages in the skin of WT and E-FABP−/− mice fed with the cocoa butter diet for 9 months. (H-I) Measurement of serum levels of IL-6 ( H ), IL-1β ( I ) and TNFα ( J .
Figure Legend Snippet: E-FABP deficiency protects high saturated fat-induced skin lesions (A) Weight of WT mice and E-FABP−/− mice before and after cocoa butter diet (45% fat) (n=16 for WT mice, and n=15/E-FABP−/− mice) and safflower diet (45% fat) (n=10/WT mice and n=15/E-FABP−/−) for 6 months. ( B ) The incidence of skin lesions in WT and E-FABP−/− mice fed with cocoa butter diet or safflower oil diet for 9 months. (C-D) Confocal analysis of CD11c+ macrophage infiltration (green color) in the skin tissue of WT and E-FABP−/− mice fed with cocoa butter for 9 months. Relative CD11c fluorescent intensity is shown in panel D . (E-G) Flow cytometric analysis of CD80 ( E ), CD86 ( F ) and MHCII ( G ) expression on CD11c+ macrophages in the skin of WT and E-FABP−/− mice fed with the cocoa butter diet for 9 months. (H-I) Measurement of serum levels of IL-6 ( H ), IL-1β ( I ) and TNFα ( J .

Techniques Used: Mouse Assay, Flow Cytometry, Expressing

SA promotes expression of costimulatory molecules and production of inflammatory cytokines in M-CSF-induced bone marrow cells (A-B) Flow cytometric analyses of CD11c expression on bone marrow cells stimulated with M-CSF (20ng/ml) and indicated concentrations of SA for 48h. Average percentage of CD11c+ cells was shown in Panel B . (C-D) Realtime PCR analysis of mRNA levels of CD11c ( C ) and CD11b ( D ) in bone marrow cells after stimulation with M-CSF and SA for 48h. (E-H) Flow cytometric analysis of the mean fluorescent intensity (MFI) of MHCII ( E ), CD86 ( F ), CD80 ( G ), and CD54 ( H ) on bone marrow cells after stimulation with M-CSF and indicated SA for 48h. (J-O) Realtime PCR analysis of mRNA levels of inflammatory cytokines, including IL-6 ( J ), TNFα ( K ), IL-1β ( L ), IL-10 ( M ), IFNα ( N ) and IFNβ ( O ) in M-CSF-stimulated bone marrow cells in the presence or absence SA treatment (100μM) for 48h. (P-S) Measurement of protein levels of IL-6 ( P ), TNFα ( Q ) IL-1β ( R ) and IL-10 ( S ) in the supernatants of M-CSF-differentiated macrophages in the presence or absence SA treatment (100μM) for 48h. Data are shown as mean ± SEM (* p
Figure Legend Snippet: SA promotes expression of costimulatory molecules and production of inflammatory cytokines in M-CSF-induced bone marrow cells (A-B) Flow cytometric analyses of CD11c expression on bone marrow cells stimulated with M-CSF (20ng/ml) and indicated concentrations of SA for 48h. Average percentage of CD11c+ cells was shown in Panel B . (C-D) Realtime PCR analysis of mRNA levels of CD11c ( C ) and CD11b ( D ) in bone marrow cells after stimulation with M-CSF and SA for 48h. (E-H) Flow cytometric analysis of the mean fluorescent intensity (MFI) of MHCII ( E ), CD86 ( F ), CD80 ( G ), and CD54 ( H ) on bone marrow cells after stimulation with M-CSF and indicated SA for 48h. (J-O) Realtime PCR analysis of mRNA levels of inflammatory cytokines, including IL-6 ( J ), TNFα ( K ), IL-1β ( L ), IL-10 ( M ), IFNα ( N ) and IFNβ ( O ) in M-CSF-stimulated bone marrow cells in the presence or absence SA treatment (100μM) for 48h. (P-S) Measurement of protein levels of IL-6 ( P ), TNFα ( Q ) IL-1β ( R ) and IL-10 ( S ) in the supernatants of M-CSF-differentiated macrophages in the presence or absence SA treatment (100μM) for 48h. Data are shown as mean ± SEM (* p

Techniques Used: Expressing, Flow Cytometry, Polymerase Chain Reaction

E-FABP deficiency reduces CD11c+ macrophages in obese mice WT and E-FABP−/− mice were fed on HFD (60% fat) for 20 weeks. Different tissues or organs were collected, respectively from the obese WT and E-FABP−/− mice (n=5) for analysis of the presence of CD11b+CD11c+ macrophages. ( A-D ) Flow cytometric surface staining for analysis of CD11b+CD11c+ macrophages in bone marrow ( A ), liver ( B ), lung ( C ) and skin ( D ). Average percentage of CD11c+ cells is shown in the right panel. (E-G) Measurement of cytokine levels of IL-6 ( E ), IL-1β ( F ) and TNFα ( G .
Figure Legend Snippet: E-FABP deficiency reduces CD11c+ macrophages in obese mice WT and E-FABP−/− mice were fed on HFD (60% fat) for 20 weeks. Different tissues or organs were collected, respectively from the obese WT and E-FABP−/− mice (n=5) for analysis of the presence of CD11b+CD11c+ macrophages. ( A-D ) Flow cytometric surface staining for analysis of CD11b+CD11c+ macrophages in bone marrow ( A ), liver ( B ), lung ( C ) and skin ( D ). Average percentage of CD11c+ cells is shown in the right panel. (E-G) Measurement of cytokine levels of IL-6 ( E ), IL-1β ( F ) and TNFα ( G .

Techniques Used: Mouse Assay, Flow Cytometry, Staining

14) Product Images from "Proinflammatory α-Adrenergic Neuronal Regulation of Splenic IFN-γ, IL-6, and TGF-β of Mice from Day 15 onwards in Arthritis"

Article Title: Proinflammatory α-Adrenergic Neuronal Regulation of Splenic IFN-γ, IL-6, and TGF-β of Mice from Day 15 onwards in Arthritis

Journal: Neuroimmunomodulation

doi: 10.1159/000508109

Effects of electrically released neurotransmitters on cytokine secretion (IFN-γ, IL-6, and TGF-β). The individual panels show control conditions (Co, white boxes) and conditions under electrical stimulation (ES, red boxes) on days 14, 32, and 55 during arthritis. p values compare groups using Mann-Whitney U test statistics. Data are given as box-plots with the 10th (whisker), 25th, 50th (median), 75th, and 90th (whisker) percentiles. For each condition, at least 25 mice (200 spleen slices) were used.
Figure Legend Snippet: Effects of electrically released neurotransmitters on cytokine secretion (IFN-γ, IL-6, and TGF-β). The individual panels show control conditions (Co, white boxes) and conditions under electrical stimulation (ES, red boxes) on days 14, 32, and 55 during arthritis. p values compare groups using Mann-Whitney U test statistics. Data are given as box-plots with the 10th (whisker), 25th, 50th (median), 75th, and 90th (whisker) percentiles. For each condition, at least 25 mice (200 spleen slices) were used.

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

Neuronal adrenergic regulation of IL-6 during arthritis. The graph shows β-adrenergic ( a ), α 1 -adrenergic ( b ), and α2-adrenergic ( c ) effects. The individual panels show control conditions (Co, white boxes), conditions under electrical stimulation (ES, red boxes), and conditions under ES + antagonist (grey boxes) on days 14, 32, and 55 in the course of arthritis. The blue boxes demonstrate the significant effects of the respective antagonist in relation to ES alone ( p values are given). # p
Figure Legend Snippet: Neuronal adrenergic regulation of IL-6 during arthritis. The graph shows β-adrenergic ( a ), α 1 -adrenergic ( b ), and α2-adrenergic ( c ) effects. The individual panels show control conditions (Co, white boxes), conditions under electrical stimulation (ES, red boxes), and conditions under ES + antagonist (grey boxes) on days 14, 32, and 55 in the course of arthritis. The blue boxes demonstrate the significant effects of the respective antagonist in relation to ES alone ( p values are given). # p

Techniques Used:

15) Product Images from "Anti-Inflammatory Oleanolic Triterpenes from Chinese Acorns"

Article Title: Anti-Inflammatory Oleanolic Triterpenes from Chinese Acorns

Journal: Molecules

doi: 10.3390/molecules21050669

Compound 1 inhibited TNF-α-induced IL-6 and IL-8 production (* p
Figure Legend Snippet: Compound 1 inhibited TNF-α-induced IL-6 and IL-8 production (* p

Techniques Used:

16) Product Images from "Function of GRIM-19, a Mitochondrial Respiratory Chain Complex I Protein, in Innate Immunity *"

Article Title: Function of GRIM-19, a Mitochondrial Respiratory Chain Complex I Protein, in Innate Immunity *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M112.340315

Decreased IL-12 production in GRIM-19 +/− BMDMs. A–D , BMDMs from WT and GRIM-19 +/− mice were infected with S. saprophyticus ( SS ) or stimulated with LPS alone (10 ng/ml) or with MDP (10 μg/ml) for 6 or 20 h. The cell culture medium was harvested to check the production of IL-6 ( A ), IL-12 ( B ), IL-10 ( C ), and TNF-α ( D ) by ELISA. E and F , BMDMs from WT and GRIM-19 +/− mice were infected with S. saprophyticus for 6 h. Total RNA were isolated and used for measuring various cytokine gene expressions by RT-PCR ( E ) and real-time RT-PCR ( F ). Relative gene expression indicates the -folds of increase in comparison with the basal level expression of WT and GRIM-19 +/− BMDMs without treatment in F. Error bars in panels A–D and F indicate S.D.
Figure Legend Snippet: Decreased IL-12 production in GRIM-19 +/− BMDMs. A–D , BMDMs from WT and GRIM-19 +/− mice were infected with S. saprophyticus ( SS ) or stimulated with LPS alone (10 ng/ml) or with MDP (10 μg/ml) for 6 or 20 h. The cell culture medium was harvested to check the production of IL-6 ( A ), IL-12 ( B ), IL-10 ( C ), and TNF-α ( D ) by ELISA. E and F , BMDMs from WT and GRIM-19 +/− mice were infected with S. saprophyticus for 6 h. Total RNA were isolated and used for measuring various cytokine gene expressions by RT-PCR ( E ) and real-time RT-PCR ( F ). Relative gene expression indicates the -folds of increase in comparison with the basal level expression of WT and GRIM-19 +/− BMDMs without treatment in F. Error bars in panels A–D and F indicate S.D.

Techniques Used: Mouse Assay, Infection, Cell Culture, Enzyme-linked Immunosorbent Assay, Isolation, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Expressing

17) Product Images from "Phosphorylation-dependent Regnase-1 release from endoplasmic reticulum is critical in IL-17 response"

Article Title: Phosphorylation-dependent Regnase-1 release from endoplasmic reticulum is critical in IL-17 response

Journal: The Journal of Experimental Medicine

doi: 10.1084/jem.20181078

Regnase-1 phosphorylation results in attenuation of its degradation of IL-6 mRNA. (A) Immunoblotting analysis of Regnase-1 (Reg1; i) and quantitative PCR (qPCR) analysis of IL-6 mRNA (ii). WT MEFs sequentially stimulated with TNF-α for 2 h, followed by IL-17A for 0–4 h. qPCR data were collected from three independent experiments. ***, P
Figure Legend Snippet: Regnase-1 phosphorylation results in attenuation of its degradation of IL-6 mRNA. (A) Immunoblotting analysis of Regnase-1 (Reg1; i) and quantitative PCR (qPCR) analysis of IL-6 mRNA (ii). WT MEFs sequentially stimulated with TNF-α for 2 h, followed by IL-17A for 0–4 h. qPCR data were collected from three independent experiments. ***, P

Techniques Used: Real-time Polymerase Chain Reaction

18) Product Images from "Targeting Toll-like Receptor (TLR) Signaling by Toll/Interleukin-1 Receptor (TIR) Domain-containing Adapter Protein/MyD88 Adapter-like (TIRAP/Mal)-derived Decoy Peptides *"

Article Title: Targeting Toll-like Receptor (TLR) Signaling by Toll/Interleukin-1 Receptor (TIR) Domain-containing Adapter Protein/MyD88 Adapter-like (TIRAP/Mal)-derived Decoy Peptides *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M112.360925

Effect of select TIRAP decoy peptides on TNF-α and IL-6 in mouse blood following intraperitoneal injection of LPS. C57BL/6J mice were injected with peptide TR5, TR6, or TR7 or mock-treated 1 h before injection of purified E. coli LPS. Peptides and LPS were injected intraperitoneally at 10 nmol/g or 1 μg/g of animal weight, respectively.
Figure Legend Snippet: Effect of select TIRAP decoy peptides on TNF-α and IL-6 in mouse blood following intraperitoneal injection of LPS. C57BL/6J mice were injected with peptide TR5, TR6, or TR7 or mock-treated 1 h before injection of purified E. coli LPS. Peptides and LPS were injected intraperitoneally at 10 nmol/g or 1 μg/g of animal weight, respectively.

Techniques Used: Injection, Mouse Assay, Purification

Effect of TIRAP decoy peptides on TLR2 signaling. Mouse macrophages were incubated in the presence of 20 ( black bars ) or 40 ( white bars ) μ m decoy peptide for 30 min prior to stimulation with P3C (500 ng/ml; A and C ) or P2C (50 ng/ml; B ). Cytokine mRNA expression was measured 1 h after TLR2 stimulation and is normalized to expression of the hypoxanthine phosphoribosyltransferase gene. C , IL-6 and TNF-α were measured by ELISA in macrophage supernatants collected 5 h after P3C (500 ng/ml) stimulation. D , ERK phosphorylation was measured by Western analysis in primary macrophage stimulated with P3C for 30 min. CP , control peptide.
Figure Legend Snippet: Effect of TIRAP decoy peptides on TLR2 signaling. Mouse macrophages were incubated in the presence of 20 ( black bars ) or 40 ( white bars ) μ m decoy peptide for 30 min prior to stimulation with P3C (500 ng/ml; A and C ) or P2C (50 ng/ml; B ). Cytokine mRNA expression was measured 1 h after TLR2 stimulation and is normalized to expression of the hypoxanthine phosphoribosyltransferase gene. C , IL-6 and TNF-α were measured by ELISA in macrophage supernatants collected 5 h after P3C (500 ng/ml) stimulation. D , ERK phosphorylation was measured by Western analysis in primary macrophage stimulated with P3C for 30 min. CP , control peptide.

Techniques Used: Incubation, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot

19) Product Images from "Polymer scaffold architecture is a key determinant in mast cell inflammatory and angiogenic responses"

Article Title: Polymer scaffold architecture is a key determinant in mast cell inflammatory and angiogenic responses

Journal: Journal of biomedical materials research. Part A

doi: 10.1002/jbm.a.36605

I ncreasing pore size of 60 mg/mL electrospun scaffolds suppresses IL-6 and TNF production. (A) Fiber and pore diameters of the indicated scaffolds were calculated from SEM images shown at right. Data shown are mean ± SEM of 60 measurements. (B) Representative electromicrographs of a 60AF scaffold at two magnifications, showing regions of increased porosity. (C) BMMC were seeded on fibronectin-coated 60 and 60 AF electrospun scaffolds for 48 h and then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for IL-6 and TNF. Results are presented as mean ± SEM of nine samples from three independent experiments. ****, p
Figure Legend Snippet: I ncreasing pore size of 60 mg/mL electrospun scaffolds suppresses IL-6 and TNF production. (A) Fiber and pore diameters of the indicated scaffolds were calculated from SEM images shown at right. Data shown are mean ± SEM of 60 measurements. (B) Representative electromicrographs of a 60AF scaffold at two magnifications, showing regions of increased porosity. (C) BMMC were seeded on fibronectin-coated 60 and 60 AF electrospun scaffolds for 48 h and then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for IL-6 and TNF. Results are presented as mean ± SEM of nine samples from three independent experiments. ****, p

Techniques Used: Enzyme-linked Immunosorbent Assay

Decreasing pore size of 140 mg/mL electrospun scaffolds has little effect on IL-6 and TNF production. (A) Fiber and pore diameters of the indicated scaffolds were calculated from SEM images. Fiber diameter was calculated from 25 to 40 measures; pore diameter is from 60 measurements. (B) Representative electromicrograph of a 140C scaffold. (C) BMMC were seeded on fibronectin-coated 140 and 140C electrospun scaffolds for 48 h and then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for IL-6 and TNF. Results are presented as mean ± SEM of nine samples from three independent experiments. *, p
Figure Legend Snippet: Decreasing pore size of 140 mg/mL electrospun scaffolds has little effect on IL-6 and TNF production. (A) Fiber and pore diameters of the indicated scaffolds were calculated from SEM images. Fiber diameter was calculated from 25 to 40 measures; pore diameter is from 60 measurements. (B) Representative electromicrograph of a 140C scaffold. (C) BMMC were seeded on fibronectin-coated 140 and 140C electrospun scaffolds for 48 h and then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for IL-6 and TNF. Results are presented as mean ± SEM of nine samples from three independent experiments. *, p

Techniques Used: Enzyme-linked Immunosorbent Assay

Mast cell IL-6 and TNF production is altered on scaffolds of different morphologies. (A, B) BMMC were seeded on fibronectin-coated electrospun scaffolds for 48 h, then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for (A) IL-6 and TNF or (B) MCP-1 and MIP-1α. Results are mean ± SEM of 6–15 samples from two to three independent experiments. (C) BMMC were seeded and activated as in (A). RNA was harvested 3 h after activation and analyzed by RT-qPCR to detect mRNA for IL-6 and TNF. Results are mean ± SEM of 8–12 samples from two independent experiments.*, p
Figure Legend Snippet: Mast cell IL-6 and TNF production is altered on scaffolds of different morphologies. (A, B) BMMC were seeded on fibronectin-coated electrospun scaffolds for 48 h, then activated with LPS (1 μg/mL) or IL-33 (100 ng/mL). Supernatants were collected 16 h later and analyzed via ELISA for (A) IL-6 and TNF or (B) MCP-1 and MIP-1α. Results are mean ± SEM of 6–15 samples from two to three independent experiments. (C) BMMC were seeded and activated as in (A). RNA was harvested 3 h after activation and analyzed by RT-qPCR to detect mRNA for IL-6 and TNF. Results are mean ± SEM of 8–12 samples from two independent experiments.*, p

Techniques Used: Enzyme-linked Immunosorbent Assay, Activation Assay, Quantitative RT-PCR

Related Articles

Enzyme-linked Immunosorbent Assay:

Article Title: Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485
Article Snippet: .. To measure secreted cytokines, supernatants were harvested after 6 h and tested for their levels of cytokines using ELISAs with Mouse IL-6 and TNF-α ELISA MAX Deluxe kits (BioLegend, San Diego, CA, USA) according to the manufacturer's instructions. .. Cell number monitoring was assessed using a Cell Counting Kit-8 incorporating WST-8 (2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodium salt) (Dojindo Molecular Technologies, Rockville, MD, USA).

Article Title: Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice
Article Snippet: .. The levels of IL-1β, IL-6, CXCL1, TNF-α, and IL-10 were measured in BAL supernatant by using commercially available ELISA kits according to the manufacturer's instructions: IL-1β (#43601; BioLegend), IL-6 (#431301; BioLegend), CXCL1 (#DY453; R & D), TNF-α (#430901; BioLegend), IL-10 (#431411; BioLegend). .. Paraffin sections (5 μm) were placed on slides and stained with hematoxylin and eosin to quantify the number of neutrophils in the lung parenchyma.

Article Title: Lysozyme from hen egg white ameliorates lipopolysaccharide-induced systemic inflammation in mice
Article Snippet: .. The concentrations of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in samples were measured by enzyme-linked immunosorbent assay (ELISA) using mouse IL-6 ELISA kit (BioLegend, San Diego, CA, USA) and mouse TNF-α ELISA kit (eBioscience, San Diego, CA, USA), respectively, according to the manufacturer’s instructions. ..

Article Title: Early Secreted Antigenic Target of 6-kDa of Mycobacterium tuberculosis Stimulates IL-6 Production by Macrophages through Activation of STAT3
Article Snippet: .. Determination of IL-6 concentration IL-6 levels in the culture supernatants were determined by Human IL-6 ELISA MAXTM Standard or mouse IL-6 ELISA MAXTM Standard (both from Biolegend) following the manufacturer’s instructions. ..

Article Title: Gut microbial metabolites alter IgA immunity in type 1 diabetes
Article Snippet: .. Cytokine ELISA.Murine IL-6 was measured using the Mouse IL-6 ELISA kit following the manufacturer’s instructions (BioLegend). .. Real-time qPCR.

Article Title: Mycolactone displays anti-inflammatory effects on the nervous system
Article Snippet: .. The release of CCL2, IL-6 and TNF-α into culture supernatant was assessed by ELISA using respectively the mouse CCL2 Uncoated ELISA kit (ThermoFisher scientific, 88-7391-22) and the mouse IL-6 and TNF-α ELISA MAX kits (Biolegend, 431301 and 430904). .. For IL-6 ELISA assay on SCs, SCs were seeded at 2 x 104 in 24 well plates coated with poly-L-Lysin.

Article Title: Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
Article Snippet: .. ELISA ELISAs were performed to measure human IL-1β, human IL-10, human IL-12, mouse IL-6, mouse IL-10, and mouse IL-12 using Human IL-1β ELISA Ready-SET-Go!, Human IL-10 ELISA Ready-SET-Go!, Human IL-12 ELISA Ready-SET-Go! (eBioscience, San Diego, CA), Mouse IL-6 ELISA MAX standard, Mouse IL-10 ELISA MAX standard, and Mouse IL-12 ELISA MAX standard, respectively (BioLegend). .. All ELISAs were performed using 96-well half-area microplates (Greiner) according to the manufacturer's directions.

Concentration Assay:

Article Title: Early Secreted Antigenic Target of 6-kDa of Mycobacterium tuberculosis Stimulates IL-6 Production by Macrophages through Activation of STAT3
Article Snippet: .. Determination of IL-6 concentration IL-6 levels in the culture supernatants were determined by Human IL-6 ELISA MAXTM Standard or mouse IL-6 ELISA MAXTM Standard (both from Biolegend) following the manufacturer’s instructions. ..

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    BioLegend il 12p40
    DNA-PKcs is involved in the IL-6 and IL-12 response to CpG-ODN. Bone marrow-derived dendritic cells (DCs) from WT, DNA-PKcs −/− , TLR9 −/− and DNA-PKcs −/−/ TLR9 −/− mice were harvested based on their natural status: adhesion and suspension. ( A ). Combined DCs (adhesion and suspension) at day 7.5 were subjected to flow cytometry. The levels of CD11b, CD11c and MHC-II expression on DCs were determined. ( B–M ). Adhesion or suspension DCs at day 6.5 were seeded in 96-well plates at 1×10 5 /well in triplicate, and then treated with CpG-ODN (CpG, 0.2, 0.73, 2.2 or 7.3 µg/ml), LPS (0.1 µg/ml), R848 (0.125 µg/ml), or left untreated for indicated time durations. The levels of IL-6 ( B–G ) and <t>IL-12p40</t> ( H–M ) were determined by ELISA using IL-6 or IL-12p40 ELISA kits. Similar results were obtained in at least 3 independent experiments. Note: bars represent the average of triplicates ± SD. * p
    Il 12p40, supplied by BioLegend, used in various techniques. Bioz Stars score: 93/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    BioLegend anti il 4 antibody
    Hematoxylin and eosin staining of paws from mice that received various treatments. (a) Ankle joint (clinical score 0) from a mouse that received rat IgG control antibody demonstrates a mild inflammatory infiltrate within a non-distorted joint space. A mild degree of synovial hyperplasia is also present. No significant cartilage or bone destruction is seen (hematoxylin and eosin, 20 ×). (b) Arthritic joint (clinical score 4) from a mouse that received anti-IFN-γ antibody, demonstrating inflammatory cells, with partial filling of the joint space. Mild synovial hyperplasia is present along with early, minimal alteration of cartilage. Inflammatory changes extend into the adjacent soft tissue. No significant bony changes are present and the joint space is otherwise intact (hematoxylin and eosin, 10 ×). (c) Arthritic joint (clinical score 4) from a mouse that received neutralizing antibodies to IFN-γ + <t>IL-4,</t> demonstrating severe inflammatory changes including complete filling of the joint space and extension to the soft tissue. Cartilage is significantly destroyed and the bone shows a substantial amount of destruction and remodeling (hematoxylin and eosin, 10 ×).
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    BioLegend tnf α
    GM-CSF boosts LPS-induced IL-1 secretion. (A) CD11b + fraction of FLT3L derived DCs was stimulated 24 h with a wide range of different LPS concentrations (0.001–10 µg/ml) in absence (white circles) or presence of 5 ng/ml GM-CSF (black circles). 5 mM ATP was added as a danger signal. Released IL-1β, IL-1α, <t>TNF-α</t> and IL-6 were measured in the culture supernatants by standard ELISA and each value represents the mean of triplicates +/− SD. (B) CD11b + fraction of FLT3L generated DCs was primed for 24 h with 100 ng/ml LPS with (back bars) or without (white bars) 5 ng/ml GM-CSF and stimulated with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU, 200 µg/ml Alu). Each bar represents the mean of triplicates +/− SD. (C) CD11b + fraction of FLT3L generated DCs was primed with TLR agonists (100 ng/ml LPS and Pam 3 CSK 4 ), Dectin agonist, Curdlan (100 µg/ml) and pro-inflammatory cytokine TNF-α (100 ng/ml) in absence (white bars) or presence (back bars) of 5 ng/ml GM-CSF and stimulated subsequently with ATP. Each bar represents the mean of triplicates +/− SD. (D) GM-CSF derived BM DCs, M-CSF-derived BM MØ as well as L929-derived BM MØ were compared to the CD11b + fraction of FLT3L-derived DCs for their capacity to secrete IL-1β upon 24 h LPS stimulation (100 ng/ml) in absence or in presence of GM-CSF (5 ng/ml). ATP was added as danger signal. Both, WT (black bars) and GM-CSF R−/− cells (white bars) were tested. Each bar represents the mean of triplicates +/− SD. All results are representative of at least two independent experiments.
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    BioLegend mouse il 6
    Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, <t>IL-6,</t> IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P
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    DNA-PKcs is involved in the IL-6 and IL-12 response to CpG-ODN. Bone marrow-derived dendritic cells (DCs) from WT, DNA-PKcs −/− , TLR9 −/− and DNA-PKcs −/−/ TLR9 −/− mice were harvested based on their natural status: adhesion and suspension. ( A ). Combined DCs (adhesion and suspension) at day 7.5 were subjected to flow cytometry. The levels of CD11b, CD11c and MHC-II expression on DCs were determined. ( B–M ). Adhesion or suspension DCs at day 6.5 were seeded in 96-well plates at 1×10 5 /well in triplicate, and then treated with CpG-ODN (CpG, 0.2, 0.73, 2.2 or 7.3 µg/ml), LPS (0.1 µg/ml), R848 (0.125 µg/ml), or left untreated for indicated time durations. The levels of IL-6 ( B–G ) and IL-12p40 ( H–M ) were determined by ELISA using IL-6 or IL-12p40 ELISA kits. Similar results were obtained in at least 3 independent experiments. Note: bars represent the average of triplicates ± SD. * p

    Journal: PLoS ONE

    Article Title: Involvement of DNA-PKcs in the IL-6 and IL-12 Response to CpG-ODN Is Mediated by Its Interaction with TRAF6 in Dendritic Cells

    doi: 10.1371/journal.pone.0058072

    Figure Lengend Snippet: DNA-PKcs is involved in the IL-6 and IL-12 response to CpG-ODN. Bone marrow-derived dendritic cells (DCs) from WT, DNA-PKcs −/− , TLR9 −/− and DNA-PKcs −/−/ TLR9 −/− mice were harvested based on their natural status: adhesion and suspension. ( A ). Combined DCs (adhesion and suspension) at day 7.5 were subjected to flow cytometry. The levels of CD11b, CD11c and MHC-II expression on DCs were determined. ( B–M ). Adhesion or suspension DCs at day 6.5 were seeded in 96-well plates at 1×10 5 /well in triplicate, and then treated with CpG-ODN (CpG, 0.2, 0.73, 2.2 or 7.3 µg/ml), LPS (0.1 µg/ml), R848 (0.125 µg/ml), or left untreated for indicated time durations. The levels of IL-6 ( B–G ) and IL-12p40 ( H–M ) were determined by ELISA using IL-6 or IL-12p40 ELISA kits. Similar results were obtained in at least 3 independent experiments. Note: bars represent the average of triplicates ± SD. * p

    Article Snippet: The supernatants were collected and the production of IL-6 or IL-12p40 was determined by enzyme-linked immunosorbent assay (ELISA) kits (Biolegend) based on the manufacturer’s instruction.

    Techniques: Derivative Assay, Mouse Assay, Flow Cytometry, Cytometry, Expressing, Enzyme-linked Immunosorbent Assay

    Hematoxylin and eosin staining of paws from mice that received various treatments. (a) Ankle joint (clinical score 0) from a mouse that received rat IgG control antibody demonstrates a mild inflammatory infiltrate within a non-distorted joint space. A mild degree of synovial hyperplasia is also present. No significant cartilage or bone destruction is seen (hematoxylin and eosin, 20 ×). (b) Arthritic joint (clinical score 4) from a mouse that received anti-IFN-γ antibody, demonstrating inflammatory cells, with partial filling of the joint space. Mild synovial hyperplasia is present along with early, minimal alteration of cartilage. Inflammatory changes extend into the adjacent soft tissue. No significant bony changes are present and the joint space is otherwise intact (hematoxylin and eosin, 10 ×). (c) Arthritic joint (clinical score 4) from a mouse that received neutralizing antibodies to IFN-γ + IL-4, demonstrating severe inflammatory changes including complete filling of the joint space and extension to the soft tissue. Cartilage is significantly destroyed and the bone shows a substantial amount of destruction and remodeling (hematoxylin and eosin, 10 ×).

    Journal: Arthritis Research & Therapy

    Article Title: Regulation of pathogenic IL-17 responses in collagen-induced arthritis: roles of endogenous interferon-gamma and IL-4

    doi: 10.1186/ar2838

    Figure Lengend Snippet: Hematoxylin and eosin staining of paws from mice that received various treatments. (a) Ankle joint (clinical score 0) from a mouse that received rat IgG control antibody demonstrates a mild inflammatory infiltrate within a non-distorted joint space. A mild degree of synovial hyperplasia is also present. No significant cartilage or bone destruction is seen (hematoxylin and eosin, 20 ×). (b) Arthritic joint (clinical score 4) from a mouse that received anti-IFN-γ antibody, demonstrating inflammatory cells, with partial filling of the joint space. Mild synovial hyperplasia is present along with early, minimal alteration of cartilage. Inflammatory changes extend into the adjacent soft tissue. No significant bony changes are present and the joint space is otherwise intact (hematoxylin and eosin, 10 ×). (c) Arthritic joint (clinical score 4) from a mouse that received neutralizing antibodies to IFN-γ + IL-4, demonstrating severe inflammatory changes including complete filling of the joint space and extension to the soft tissue. Cartilage is significantly destroyed and the bone shows a substantial amount of destruction and remodeling (hematoxylin and eosin, 10 ×).

    Article Snippet: Plates were coated with anti-IFN-γ antibody (clone R46A2 or XMG1.2, Biolegend, San Diego, CA, USA), anti-IL-4 antibody (clone11B11) or anti-IL-17 antibody (clone TC11-18H10.1, Biolegend, San Diego, CA, USA).

    Techniques: Staining, Mouse Assay

    Regulation of IL-17 responses by Th2 cytokine IL-4 during the initiation phase of arthritis. (a) Neutralizing antibody to IFN-γ (clone R46A2, 100 μg/mouse/day), and/or neutralizing antibody to IL-4 (clone 11B11, 100 μg/mouse/day) was administered intraperitoneally from day 10 to 20 after immunization with collagen and complete Freund's adjuvant (CFA). Rat IgG was used as isotype control. The control group did not receive any antibody. Arthritis was assessed from day 10 by clinical scoring. Data is representative of two experiments, with n = 8 in each group. * P

    Journal: Arthritis Research & Therapy

    Article Title: Regulation of pathogenic IL-17 responses in collagen-induced arthritis: roles of endogenous interferon-gamma and IL-4

    doi: 10.1186/ar2838

    Figure Lengend Snippet: Regulation of IL-17 responses by Th2 cytokine IL-4 during the initiation phase of arthritis. (a) Neutralizing antibody to IFN-γ (clone R46A2, 100 μg/mouse/day), and/or neutralizing antibody to IL-4 (clone 11B11, 100 μg/mouse/day) was administered intraperitoneally from day 10 to 20 after immunization with collagen and complete Freund's adjuvant (CFA). Rat IgG was used as isotype control. The control group did not receive any antibody. Arthritis was assessed from day 10 by clinical scoring. Data is representative of two experiments, with n = 8 in each group. * P

    Article Snippet: Plates were coated with anti-IFN-γ antibody (clone R46A2 or XMG1.2, Biolegend, San Diego, CA, USA), anti-IL-4 antibody (clone11B11) or anti-IL-17 antibody (clone TC11-18H10.1, Biolegend, San Diego, CA, USA).

    Techniques:

    Degree of tissue inflammation and bone and cartilage destruction in the absence of endogenous Th1 and Th2 cytokines. (a and b) Tissue sections of arthritic hind paw from mice that received neutralizing antibodies to IFN-γ alone, IFN-γ + IL-4, IL-4 alone, rat IgG or no antibody were stained with hematoxylin and eosin. The sections were scored for inflammatory infiltrate, synovitis, bone damage and cartilage destruction. Data are presented as mean +/- standard deviation (SD). * P

    Journal: Arthritis Research & Therapy

    Article Title: Regulation of pathogenic IL-17 responses in collagen-induced arthritis: roles of endogenous interferon-gamma and IL-4

    doi: 10.1186/ar2838

    Figure Lengend Snippet: Degree of tissue inflammation and bone and cartilage destruction in the absence of endogenous Th1 and Th2 cytokines. (a and b) Tissue sections of arthritic hind paw from mice that received neutralizing antibodies to IFN-γ alone, IFN-γ + IL-4, IL-4 alone, rat IgG or no antibody were stained with hematoxylin and eosin. The sections were scored for inflammatory infiltrate, synovitis, bone damage and cartilage destruction. Data are presented as mean +/- standard deviation (SD). * P

    Article Snippet: Plates were coated with anti-IFN-γ antibody (clone R46A2 or XMG1.2, Biolegend, San Diego, CA, USA), anti-IL-4 antibody (clone11B11) or anti-IL-17 antibody (clone TC11-18H10.1, Biolegend, San Diego, CA, USA).

    Techniques: Mouse Assay, Staining, Standard Deviation

    Effect of neutralization of IL-17 in the presence or absence of anti-IFN-γ and/or anti-IL-4 during the initiation phase of arthritis. (a) Neutralizing antibody to IFN-γ (clone R46A2, 100 μg/mouse/day), and/or neutralizing antibody to IL-4 (clone 11B11, 100 μg/mouse/day), and neutralizing antibody to IL-17 (clone M210, 100 μg/mouse/day) was administered intraperitoneally from day 10 to 20 after immunization with collagen and complete Freund's adjuvant (CFA). Rat IgG was used as isotype control. The control group did not receive any antibody. Arthritis was assessed from day 10 by clinical scoring. n = 8 to 9/group. * P

    Journal: Arthritis Research & Therapy

    Article Title: Regulation of pathogenic IL-17 responses in collagen-induced arthritis: roles of endogenous interferon-gamma and IL-4

    doi: 10.1186/ar2838

    Figure Lengend Snippet: Effect of neutralization of IL-17 in the presence or absence of anti-IFN-γ and/or anti-IL-4 during the initiation phase of arthritis. (a) Neutralizing antibody to IFN-γ (clone R46A2, 100 μg/mouse/day), and/or neutralizing antibody to IL-4 (clone 11B11, 100 μg/mouse/day), and neutralizing antibody to IL-17 (clone M210, 100 μg/mouse/day) was administered intraperitoneally from day 10 to 20 after immunization with collagen and complete Freund's adjuvant (CFA). Rat IgG was used as isotype control. The control group did not receive any antibody. Arthritis was assessed from day 10 by clinical scoring. n = 8 to 9/group. * P

    Article Snippet: Plates were coated with anti-IFN-γ antibody (clone R46A2 or XMG1.2, Biolegend, San Diego, CA, USA), anti-IL-4 antibody (clone11B11) or anti-IL-17 antibody (clone TC11-18H10.1, Biolegend, San Diego, CA, USA).

    Techniques: Neutralization

    GM-CSF boosts LPS-induced IL-1 secretion. (A) CD11b + fraction of FLT3L derived DCs was stimulated 24 h with a wide range of different LPS concentrations (0.001–10 µg/ml) in absence (white circles) or presence of 5 ng/ml GM-CSF (black circles). 5 mM ATP was added as a danger signal. Released IL-1β, IL-1α, TNF-α and IL-6 were measured in the culture supernatants by standard ELISA and each value represents the mean of triplicates +/− SD. (B) CD11b + fraction of FLT3L generated DCs was primed for 24 h with 100 ng/ml LPS with (back bars) or without (white bars) 5 ng/ml GM-CSF and stimulated with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU, 200 µg/ml Alu). Each bar represents the mean of triplicates +/− SD. (C) CD11b + fraction of FLT3L generated DCs was primed with TLR agonists (100 ng/ml LPS and Pam 3 CSK 4 ), Dectin agonist, Curdlan (100 µg/ml) and pro-inflammatory cytokine TNF-α (100 ng/ml) in absence (white bars) or presence (back bars) of 5 ng/ml GM-CSF and stimulated subsequently with ATP. Each bar represents the mean of triplicates +/− SD. (D) GM-CSF derived BM DCs, M-CSF-derived BM MØ as well as L929-derived BM MØ were compared to the CD11b + fraction of FLT3L-derived DCs for their capacity to secrete IL-1β upon 24 h LPS stimulation (100 ng/ml) in absence or in presence of GM-CSF (5 ng/ml). ATP was added as danger signal. Both, WT (black bars) and GM-CSF R−/− cells (white bars) were tested. Each bar represents the mean of triplicates +/− SD. All results are representative of at least two independent experiments.

    Journal: PLoS ONE

    Article Title: GM-CSF Signalling Boosts Dramatically IL-1Production

    doi: 10.1371/journal.pone.0023025

    Figure Lengend Snippet: GM-CSF boosts LPS-induced IL-1 secretion. (A) CD11b + fraction of FLT3L derived DCs was stimulated 24 h with a wide range of different LPS concentrations (0.001–10 µg/ml) in absence (white circles) or presence of 5 ng/ml GM-CSF (black circles). 5 mM ATP was added as a danger signal. Released IL-1β, IL-1α, TNF-α and IL-6 were measured in the culture supernatants by standard ELISA and each value represents the mean of triplicates +/− SD. (B) CD11b + fraction of FLT3L generated DCs was primed for 24 h with 100 ng/ml LPS with (back bars) or without (white bars) 5 ng/ml GM-CSF and stimulated with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU, 200 µg/ml Alu). Each bar represents the mean of triplicates +/− SD. (C) CD11b + fraction of FLT3L generated DCs was primed with TLR agonists (100 ng/ml LPS and Pam 3 CSK 4 ), Dectin agonist, Curdlan (100 µg/ml) and pro-inflammatory cytokine TNF-α (100 ng/ml) in absence (white bars) or presence (back bars) of 5 ng/ml GM-CSF and stimulated subsequently with ATP. Each bar represents the mean of triplicates +/− SD. (D) GM-CSF derived BM DCs, M-CSF-derived BM MØ as well as L929-derived BM MØ were compared to the CD11b + fraction of FLT3L-derived DCs for their capacity to secrete IL-1β upon 24 h LPS stimulation (100 ng/ml) in absence or in presence of GM-CSF (5 ng/ml). ATP was added as danger signal. Both, WT (black bars) and GM-CSF R−/− cells (white bars) were tested. Each bar represents the mean of triplicates +/− SD. All results are representative of at least two independent experiments.

    Article Snippet: Cytokine measurements Cells were stimulated overnight with LPS with or without GM-CSF and subsequently treated for 1 h or 6 h with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU and 200 µg/ml Alum) and cell supernatant was analysed for IL-6, TNF-α, IL-1α and -β by ELISA following manufactures instructions (Biolegend).

    Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay, Generated

    CD11b + fraction of FLT3L derived DCs were stimulated for 3, 6, 9 and 24 h respectively with LPS alone (white bars) or in combination with GM-CSF (black bars). For the detection of IL-1β, 4×10 5 cells were stimulated for 1 h with ATP, for IL-6 and TNF-α the cytokine release of 1×10 5 cells was analysed without ATP treatment. Released cytokines were measured by ELISA. Each bar represents the mean of triplicates +/− SD.

    Journal: PLoS ONE

    Article Title: GM-CSF Signalling Boosts Dramatically IL-1Production

    doi: 10.1371/journal.pone.0023025

    Figure Lengend Snippet: CD11b + fraction of FLT3L derived DCs were stimulated for 3, 6, 9 and 24 h respectively with LPS alone (white bars) or in combination with GM-CSF (black bars). For the detection of IL-1β, 4×10 5 cells were stimulated for 1 h with ATP, for IL-6 and TNF-α the cytokine release of 1×10 5 cells was analysed without ATP treatment. Released cytokines were measured by ELISA. Each bar represents the mean of triplicates +/− SD.

    Article Snippet: Cytokine measurements Cells were stimulated overnight with LPS with or without GM-CSF and subsequently treated for 1 h or 6 h with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU and 200 µg/ml Alum) and cell supernatant was analysed for IL-6, TNF-α, IL-1α and -β by ELISA following manufactures instructions (Biolegend).

    Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay

    GM-CSF R−/− mice survive LPS-induced septic shock. (A) Survival of WT and GM-CSFR−/− mice ( n = 12 each group) injected i.p. with 50 µg/g body weight LPS. (B) WT and GM-CSFR−/− mice were bled from the retro-orbital plexus 3 h after LPS treatment. Pro-inflammatory cytokines such as IL-1α, IL-1β, IL-6 and TNF-α were measured in the serum by ELISA. The data represent the mean +/− SD of three pooled independent experiments. *

    Journal: PLoS ONE

    Article Title: GM-CSF Signalling Boosts Dramatically IL-1Production

    doi: 10.1371/journal.pone.0023025

    Figure Lengend Snippet: GM-CSF R−/− mice survive LPS-induced septic shock. (A) Survival of WT and GM-CSFR−/− mice ( n = 12 each group) injected i.p. with 50 µg/g body weight LPS. (B) WT and GM-CSFR−/− mice were bled from the retro-orbital plexus 3 h after LPS treatment. Pro-inflammatory cytokines such as IL-1α, IL-1β, IL-6 and TNF-α were measured in the serum by ELISA. The data represent the mean +/− SD of three pooled independent experiments. *

    Article Snippet: Cytokine measurements Cells were stimulated overnight with LPS with or without GM-CSF and subsequently treated for 1 h or 6 h with different danger signals (5 mM ATP, 1 µM nigericin, 100 µg/ml MSU and 200 µg/ml Alum) and cell supernatant was analysed for IL-6, TNF-α, IL-1α and -β by ELISA following manufactures instructions (Biolegend).

    Techniques: Mouse Assay, Injection, Enzyme-linked Immunosorbent Assay

    Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, IL-6, IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P

    Journal: Stem Cell Research & Therapy

    Article Title: Human multipotent stromal cells attenuate lipopolysaccharide-induced acute lung injury in mice via secretion of tumor necrosis factor-?-induced protein 6

    doi: 10.1186/scrt68

    Figure Lengend Snippet: Proinflammatory cytokine and chemokine expression is decreased by hMSC administration . Twenty-four hours after LPS exposure, IL-1β, IL-6, IL-17, IP-10, MCP-1, MIP-1α and RANTES levels were measured by multiplex immunoassay in BAL fluid. Data are expressed as mean ± SEM (n = 6 per group). * P

    Article Snippet: The quantification of mouse IL-6 was performed with mouse IL-6 ELISA MAX™ Deluxe Set from BioLegend (San Diego, CA, USA) according to the manufacturer's instruction.

    Techniques: Expressing, Multiplex Assay