[肠道微生物群与炎症性肠病]

[Gut microbiota and IBD].

作者信息

Seksik P

机构信息

Gastroenterology and Nutrition Department, Hôpital Saint Antoine, AP-HP, Paris, France.

出版信息

Gastroenterol Clin Biol. 2010 Sep;34 Suppl 1:S44-51. doi: 10.1016/S0399-8320(10)70020-8.

Abstract

Gut microbiota contains about 10(14) bacterial cells classified within 4 bacterial phyla, namely Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria. Much of the information has been generated through the application of nucleic acid-based methodologies (16S rRNA) which provide a cornerstone of microbial taxonomy. Inflammatory bowel disease (IBD) involves a dysregulated immune response to the gut microbiota in genetically predisposed hosts. Experimental animal models of colitis provide the best evidence that bacteria present in the bowel of the animals have an essential role in the pathogenesis of colitis since in most models, germ-free animals do not develop disease. Moreover, in the immunodeficient mouse model of colitis called TRUC (T-bet-/- x RAG2-/-), a colitogenic gut microbiota is selected and can be transmitted to mice with intact immunity and induce colitis. Current interest therefore focuses on the bacterial community as the source of antigens that fuel the chronic inflammation seen in IBD. Dysbiosis, an imbalance between harmful and protective bacteria, has been evoked and investigated in IBD. Thus, besides the classical pathogens, gut microbiota can drive pathogenicity via two mechanisms: an expansion of 'pro-inflammatory' species or a restriction in the protective compounds of the microbiota. Complexity of the microbiota suggests that both mechanisms may contribute to chronic gut inflammation in IBD.

摘要

肠道微生物群包含约10¹⁴个细菌细胞,分为4个细菌门,即厚壁菌门、拟杆菌门、放线菌门和变形菌门。许多信息是通过基于核酸的方法(16S rRNA)生成的,这些方法为微生物分类学奠定了基础。炎症性肠病(IBD)涉及遗传易感性宿主对肠道微生物群的免疫反应失调。结肠炎的实验动物模型提供了最佳证据,表明动物肠道中的细菌在结肠炎发病机制中起重要作用,因为在大多数模型中,无菌动物不会发病。此外,在一种名为TRUC(T-bet-/-×RAG2-/-)的结肠炎免疫缺陷小鼠模型中,可选择出具有致结肠炎作用的肠道微生物群,并可将其传播给免疫功能正常的小鼠并诱发结肠炎。因此,目前的研究重点是细菌群落,将其视为引发IBD中慢性炎症的抗原来源。IBD中已提出并研究了生态失调,即有害菌与有益菌之间的失衡。因此,除了经典病原体外,肠道微生物群可通过两种机制引发致病性:“促炎”菌的扩增或微生物群保护性化合物的减少。微生物群的复杂性表明这两种机制可能都与IBD中的慢性肠道炎症有关。

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