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目的探讨髓样细胞触发受体-2(TREM-2)对小鼠肠炎模型肠道炎症发生发展的影响。方法构建葡萄糖硫酸钠(DSS)诱导的小鼠实验性肠炎模型,采用流式细胞术检测TREM-2在炎症肠道细胞的表达,采用TREM-2敲除小鼠构建小鼠肠炎模型,检测体重、临床评分以及结肠长度,采用荧光定量PCR检测小鼠脾脏(SPs)和肠系膜淋巴(MLNs)细胞因子的表达。结果肠炎小鼠肠道TREM-2表达显著高于正常小鼠,TREM-2基因敲除肠炎小鼠体重以及结肠长度均显著高于野生型对照组,疾病临床评分(DAI)以及肠道病理评分显著低于野生型对照组小鼠,脾脏和肠系膜淋巴结的促炎性细胞因子(IFN-γ和IL-17a)表达显著低于野生型对照组小鼠(P<0.05)。结论 TREM-2增强肠道炎症反应和病理损伤,增强促炎性细胞因子分泌,从而调控炎症性肠病的发生发展,TREM-2有望成为治疗炎症性肠病的一个有效靶点。
Objective To investigate the effect of TREM-2 on intestinal inflammation in mouse enteritis model. Methods The mouse model of experimental colitis induced by sodium dodecyl sulphate (DSS) was established. The expression of TREM-2 in inflammatory gut cells was detected by flow cytometry. The murine model of mouse enteritis was established by TREM-2 knockout mice. The body weight , Clinical score and length of colon, the expression of cytokines in mouse spleen (SPs) and mesenteric lymphoid (MLNs) were detected by real-time PCR. Results The expression of TREM-2 in intestinal tract of enteritis mice was significantly higher than that of normal mice. The body weight and length of colon in TREM-2 knockout enteritis mice were significantly higher than those in wild type control group, disease clinical score (DAI) and intestinal pathological score The expression of proinflammatory cytokines (IFN-γ and IL-17a) in the spleen and mesenteric lymph nodes was significantly lower than that in wild-type control mice (P <0.05). Conclusion TREM-2 can enhance the intestinal inflammatory response and pathological injury, enhance the secretion of proinflammatory cytokines, and thus regulate the occurrence and development of inflammatory bowel disease. TREM-2 is expected to become an effective target for the treatment of inflammatory bowel disease.