title: Cytokine expression and the role of Th17 cells in a mouse model of colitis.
abstract: The aim of this study was to explore the expression of cytokines by Th17 cells and their mechanisms of action in a mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced inflammatory bowel disease (IBD). ELISA was used to detect the expression of the Th17 cytokine interleukin, (IL)-17, and that of the Th1 cytokine, interferon-γ (IFN-γ), in colon tissues. Western blot analysis was used to detect IL-17 expression in the peripheral blood mononuclear cells (PBMCs), spleen mononuclear cells (SMCs), mesenteric lymph node cells and colon tissues of the colitic mice. RT-PCR analysis was used to detect the effect of anti-IL-17 antibody application on the tumor necrosis factor (TNF)-α, IFN-γ and IL-6 mRNA levels in the SMCs of the colitic mice. The Th17 cytokine, IL-17, and the Th1 cytokine, IFN-γ, were expressed at high levels in the TNBS-induced colitic mice. In addition, the expression of the Th17 cytokine appeared earlier than that of the Th1 cytokine. The IL-17 levels in the SMCs, mesenteric lymph node cells and colon tissues of the disease model group were significantly different from those of the normal control group (p<0.01), while the IL-17 levels in the PBMCs of the disease model group were not significantly different (p>0.05) from those of the control group. Following the application of 10 µg/ml anti-IL-7 antibody, the TNF-α, IL-6 and IFN-γ mRNA levels in the SMCs of the model group demonstrated no significant differences from those of the non-antibody-treated control group (p>0.05). In conclusion, Th17 and Th1 cells are involved in TNBS-induced IBD and the effect of the Th17 cells may be mediated through the induction of the secretion of pro-inflammatory cytokines.
authors.affiliation: Shengjing Hospital of China Medical University, Shenyang, Liaoning                     110004, P.R. China.
authors.forename: Ying
authors.initials: Y
authors.lastname: He
authors.forename: Lian-Jie
authors.initials: LJ
authors.lastname: Lin
authors.forename: Chang-Qing
authors.initials: CQ
authors.lastname: Zheng
authors.forename: Yu
authors.initials: Y
authors.lastname: Jin
authors.forename: Yan
authors.initials: Y
authors.lastname: Lin
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008198:Lymph Nodes / Q000166:cytology; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000378:metabolism; D013154:Spleen / Q000166:cytology; D058504:Th17 Cells / Q000276:immunology* / Q000378:metabolism; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000906:Antibodies; D016207:Cytokines; D020381:Interleukin-17; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D014302:Trinitrobenzenesulfonic Acid