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.
Keywords: Th17 cells; Th1 cells; inflammatory bowel disease; interleukin-17; interferon-γ; tumor necrosis factor-α; interleukin-6.