Intestinal microbiota in inflammatory bowel disease: Friend of foe?
Intestinal microbiota in inflammatory bowel disease: Friend of foe?
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DOI：
10.3748/wjg.v17.i5.557
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发表时间：
2011-02-07
影响因子：
4.3
通讯作者：
Danese, Silvio
中科院分区：
文献类型：
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作者：
Fava, Francesca;Danese, Silvio
炎症性肠病(IBD)是由于对肠道共生微生物区系免疫耐受的破坏而引起的，导致遗传易感宿主的慢性肠炎和粘膜损伤。在健康个体中，肠道微生物群与宿主生物具有共生关系，并具有重要和独特的功能，包括代谢功能(即消化饮食化合物和外源物质，发酵不可消化的碳水化合物产生短链脂肪酸)，粘膜屏障功能(Le。通过抑制病原体入侵和加强上皮屏障完整性)和免疫调节功能(即粘膜免疫系统启动和维持肠上皮动态平衡)。一种微妙的平衡调节着哺乳动物与其共生细菌共存的机制。在IBD中，由于几个潜在的致病因素，这种免疫耐受机制受到损害。IBD患者的肠道微生物区系组成和活动异常，人类共生微生物区系的优势成员(即IXa和IV组梭菌、杆菌、双歧杆菌)的患病率下降，有害细菌(即硫酸盐还原细菌、大肠杆菌)增加。所观察到的生物失调伴随着先天性免疫缺陷和细菌杀伤(如粘膜防御素和IgA减少，吞噬功能障碍)和过度侵袭性适应性免疫反应(由于无效的调节性T细胞和抗原提呈细胞)，这些被认为是IBD发病的基础。然而，我们仍然不知道这些参数之间的相互作用是如何导致这种疾病的。因此，对IBD基因分型人群的肠道微生物组成、上皮完整性和粘膜免疫标记物的研究有助于阐明这一不明的发病机制。(C)2011年白石登。版权所有。
Inflammatory bowel disease (IBD) arises from disruption of immune tolerance to the gut commensal microbiota, leading to chronic intestinal inflammation and mucosal damage in genetically predisposed hosts. In healthy individuals the intestinal microbiota have a symbiotic relationship with the host organism and possess important and unique functions, including a metabolic function (i.e. digestion of dietary compounds and xenobiotics, fermentation of undigestible carbohydrates with production of short chain fatty acids), a mucosal barrier function (Le. by inhibiting pathogen invasion and strengthening epithelial barrier integrity), and an immune modulatory function (i.e. mucosal immune system priming and maintenance of intestinal epithelium homeostasis). A fine balance regulates the mechanism that allows coexistence of mammals with their commensal bacteria. In IBD this mechanism of immune tolerance is impaired because of several potential causative factors. The gut microbiota composition and activity of IBD patients are abnormal, with a decreased prevalence of dominant members of the human commensal microbiota (i.e. Clostridium IXa and IV groups, Bacterades, bifidobacteria) and a concomitant increase in detrimental bacteria (i.e. sulphate-reducing bacteria, Escherichia cob). The observed dysbiosis is concomitant with defective innate immunity and bacterial killing (i.e. reduced mucosal defensins and IgA, malfunctioning phagocytosis) and overaggressive adaptive immune response (due to ineffective regulatory T cells and antigen presenting cells), which are considered the basis of IBD pathogenesis. However, we still do not know how the interplay between these parameters causes the disease. Studies looking at gut microbial composition, epithelial integrity and mucosal immune markers in genotyped IBD populations are therefore warranted to shed light on this obscure pathogenesis. (C) 2011 Baishideng. All rights reserved.