IRF3/7在葡聚糖硫酸钠诱导结肠炎中的作用机制研究

The role of IRF3/7 in the development of dextran sodium sulfate-induced colitis

目的:研究Ⅰ型干扰素转录因子IRF3和IRF7在葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎中的作用及机制。方法:在野生型(WT)和干扰素调节因子3/7(IRF3/7)基因敲除小鼠饮水中加入DSS,5天后换正常水喂养3天,检测小鼠的生存率、体重、结肠长度及脾重等结肠炎相关指标。使用qPCR方法测定结肠炎症细胞因子及胸腺基质淋巴细胞生成素(TSLP)和白细胞介素33(IL-33)的基因表达情况,使用ELISA方法检测结肠TSLP和IL-33的蛋白表达情况。结果:IRF3/7^-/-小鼠比WT小鼠对DSS诱导产生的结肠炎更为易感,结肠组织中炎症细胞因子的表达量更高,结肠组织中TSLP与IL-33表达无明显缺陷。结论:IRF3/7对结肠炎具有保护作用,并能下调DSS诱导的结肠炎症。

Objective:To study the role of interferon transcription factors IRF3/7 in dextran sodium sulfate(DSS)-induced colitis.Methods:Wild type(WT)and IRF3/7^-/-mice were fed with DSS for 5 days,following with normal water for 3 days.The host susceptibility to colitis and the colonic expression of inflammatory cytokines,thymic stromal lymphopoietin(TSLP),and interleukin 33(IL-33)were tested by qPCR.The colonic protein level of TSLP and IL-33 were measured by ELISA.Results:IRF3/7^-/-mice were more susceptible to DSS-induced colitis than WT mice.The colonic expression of inflammatory cytokines was higher in IRF3/7^-/-mice than WT mice.However,the levels of TSLP or IL-33 in IRF3/7^-/-mice were not defective,in comparison with WT mice.Conclusions:IRF3/7 signaling pathway is critical for host to resist DSS-induced colitis in the matter which is independent of TSLP and IL-33 production.