Matricon Julien, Barnich Nicolas, Ardid Denis
Clermont Université; Université d'Auvergne; Pharmacologie Fondamentale et Clinique de la Douleur; Laboratoire de Pharmacologie Médicale; Inserm U 766; Clermont-Ferrand, France.
Self Nonself. 2010 Oct;1(4):299-309. doi: 10.4161/self.1.4.13560.
Inflammatory bowel disease (IBD) is a group of idiopathic, chronic and relapsing inflammatory conditions of the gastrointestinal tract. Familial and epidemiological studies have stressed the involvement of genetic factors and have also shown the critical role of environmental factors such as sanitation and hygiene in the development of IBD. However, the molecular mechanisms of intestinal inflammation in IBD have long remained unknown. In recent years, the study of susceptibility genes involved in the detection of bacterial components and in the regulation of the host immune response has shed light onto the potential role of intestinal pathogens and gut flora in IBD immunobiology. This review presents current knowledge on intestinal epithelial barrier alterations and on dysfunction of mucosal innate and acquired immune responses in IBD. The data support the etiological hypothesis which argues that pathogenic intestinal bacteria and/or infectious agents initiate and perpetuate the inflammation of the gut through disruption of tolerance towards the commensal microbiota in an individual with genetic vulnerability.
炎症性肠病(IBD)是一组胃肠道特发性、慢性和复发性炎症性疾病。家族性和流行病学研究强调了遗传因素的参与,也表明了环境卫生等环境因素在IBD发病过程中的关键作用。然而,IBD肠道炎症的分子机制长期以来一直不明。近年来,对参与细菌成分检测和宿主免疫反应调节的易感基因的研究,揭示了肠道病原体和肠道菌群在IBD免疫生物学中的潜在作用。本综述介绍了目前关于IBD肠道上皮屏障改变以及黏膜固有免疫和获得性免疫反应功能障碍的知识。这些数据支持了病因学假说,该假说认为致病性肠道细菌和/或感染因子通过破坏具有遗传易感性个体对共生微生物群的耐受性,引发并持续肠道炎症。