肠道缺血再灌注损伤中CD4^+ T细胞的激活及其与肠上皮细胞的相互作用

Post-ischemic gut injury is related to interaction of CD4^+ T cells and epithelial cells

目的探讨缺血后的肠道是否引起T细胞细胞因子的分泌类型改变,从而影响肠上皮细胞迁移和增殖的功能。方法将SD大鼠随机分为3组:正常对照组(n=7);I/R模型组(n=7);假手术组(n=7)。I/R模型组大鼠肠系膜上动脉夹闭60 min、再灌注24 h,取其回肠。通过免疫组化方法来分析CD4+T细胞、CD40、干扰素γ(IFNγ)和白介素4(IL-4)的表达。结果与假手术组相比,I/R模型组大鼠回肠黏膜层和黏膜下层的CD4I、FNγ和CD40表达明显增加,而IL-4的表达差异没有统计学意义。结论肠道缺血再灌注损伤可能与CD4+T细胞的激活并进一步向产生IFN-γ的Th1分化有关,而CD4+T细胞的活化可能与CD40信号途径的激活有关。

Objective To determine whether ischemia-reperfusion（I/R） changes the T cell cytokine pattern in the postischemic gut,and whether the CD4＋T cell cytokine pattern correlates with epithelial restitution.Methods Twenty-one Male Sprague-Dawley rats were divided into three groups：normal rats（n=7）,I/R rats（n=7）,and shame rats（n=7）.I/R rats received superior mesenteric artery（SMA） clamping for 60 min.After 60 min,the clamp was removed,and the SMA was allowed to be reperfused for 24hr.The expression and localization of（CD4＋）T cells,CD40,the Th1-derived cytokine interferon γ（IFNγ）,and the Th2-derived cytokine interleukin-4（IL-4） were assayed by immunohistochemistry microscope analysis on ileum harvested from rats subjected to 60 min of superior mesenteric artery occlusion and 24 h of reperfusion.Results Rats of I/R exhibited markedly increased expression of CD4,IFNγ and CD40 in ileal mucosa and submucosa.Conclusions The results indicate important roles for activation of CD4＋T cells and the induction of the IFNγ and CD40 pathways in the response to postischemic gut injury.The data also indicate that the possible beneficial effects of inhibiting IFNγ on epithelial restitution.