Strober Warren, Fuss Ivan, Mannon Peter
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.
J Clin Invest. 2007 Mar;117(3):514-21. doi: 10.1172/JCI30587.
Two broad hypotheses have arisen regarding the fundamental nature of the pathogenesis of inflammatory bowel diseases (IBDs, which include ulcerative colitis and Crohn disease). The first contends that primary dysregulation of the mucosal immune system leads to excessive immunologic responses to normal microflora. The second suggests that changes in the composition of gut microflora and/or deranged epithelial barrier function elicits pathologic responses from the normal mucosal immune system. Here we examine these hypotheses and conclude that IBD is indeed characterized by an abnormal mucosal immune response but that microbial factors and epithelial cell abnormalities can facilitate this response.
关于炎症性肠病(IBD,包括溃疡性结肠炎和克罗恩病)发病机制的基本性质,出现了两种主要假说。第一种假说认为,黏膜免疫系统的原发性失调会导致对正常微生物群产生过度免疫反应。第二种假说则表明,肠道微生物群组成的变化和/或上皮屏障功能紊乱会引发正常黏膜免疫系统的病理反应。在此,我们对这些假说进行研究,并得出结论:IBD确实具有异常黏膜免疫反应的特征,但微生物因素和上皮细胞异常会促使这种反应发生。