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.