IgG免疫复合物致小鼠肠道黏膜损伤机制的初步试验研究

摘要

目的:探讨IgG免疫复合物对小鼠肠黏膜损伤的局部组织病理特点,以及相应的细胞与分子机制,为临床上食物不耐受诱发溃疡性结肠炎的致病机制及分子诊断提供一定依据.方法:选用6周龄的BALB/c雌鼠作为实验对象进行造模,分为对照组(A组)、兔肠黏膜蛋白免疫组(B组)、DSS诱导组(C组)、兔肠黏膜蛋白免疫合并DSS诱导组(D组)共4组.造模成功后收集血清与结肠组织进行相关检测.结果:B 组小鼠血清及结肠黏膜中IgG水平上升,肠黏膜组织中少量肥大细胞活化,以及炎性细胞浸润;C组小鼠表现为典型急性溃疡性结肠炎表征,黏膜和黏膜固有层大量炎症细胞浸润,肠黏膜组织中炎症因子水平上升,黏膜上皮紧密连接减弱;D组小鼠血清及结肠黏膜中IgG水平显著升高,组织学表现与DSS诱导组相似,并有显著肥大细胞浸润与活化.结论:IgG免疫复合物通过介导肥大细胞活化脱颗粒,诱发肠黏膜上皮损伤,可能与肥大细胞释放的促炎因子导致的局部炎症以及对上皮细胞紧密连接蛋白的表达影响有关.%Objective:To study the cellular pathology and molecular mechanisms of intestinal mucosal damage induced by IgG immune complex in mice.And to explore the pathogenic mechanism and molecular diagnosis evidence of ulcerative colitis induced by food intolerance in clinical practice.Methods: Six weeks old BALB/c female mice were used to build animal model.All the mice were divided into four groups:the control group(group A),the rabbit intestinal mucosal protein immunized group(group B),the DSS induced group(group C),the rabbit intestinal mucosal protein immunized combined with DSS induced group(group D).After successful establishment of animal model,serum and colon tissues were collected to be performed relevant tests.Results: IgG level in serum and colonic mucosa of group B mice increased.And inflammatory cell infiltration and a small amount of mast cell activation were observed in intestinal mucosa;group C mice showed the typical acute ulcerative colitis:a large number of inflammatory cells infiltration,inflammatory factor levels increased in mucosa and mucosa lamina propria,and mucosal epithelial cells′ tight junction weakened;group D mice manifested both high level of IgG in serum and colonic mucosa and also typical acute ulcerative colitis.Besides,significant mast cell activation was observed in the intestinal mucosa.Conclusion: We infer from the experimental results that IgG immune complexes can induce the damage of intestinal epithelium by mediating activation of mast cells.And during the process,the level of inflammatory cytokines increased in intestinal mucosa and the expression of tight junction protein in epithelial cell decreased.These factors contribute to the promotion of intestinal mucosa damage induced by immune complexes.