Partners in Leaky Gut Syndrome: Intestinal Dysbiosis and Autoimmunity.

Partners in Leaky Gut Syndrome: Intestinal Dysbiosis and Autoimmunity.
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DOI:
10.3389/fimmu.2021.673708
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发表时间:
2021
影响因子:
7.3
通讯作者:
Hase K
Hase K
中科院分区:
医学2区
文献类型:
--
作者:
Kinashi Y;Hase K

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肠道表面组成性地暴露于多种抗原,例如食物抗原、食源性病原体和肠道微生物。肠上皮细胞具有独特的屏障功能,可防止潜在的敌对抗原易位到体内。上皮屏障的破坏增加了肠道通透性,导致漏肠综合征(LGS)。临床报告表明,LGS有助于自身免疫性疾病,如1型糖尿病,多发性硬化症,类风湿性关节炎和乳糜泻。此外,肠道微生物群在调节宿主免疫力方面起着关键作用;在自身免疫性疾病患者中观察到微生物群落的异常,称为生态失调。然而,肠道生态失调,LGS和自身免疫性疾病之间的病理联系尚未完全阐明。本文综述了目前的理解,如何肠道微生物群有助于通过修改上皮屏障的自身免疫性疾病的发病机制。
The intestinal surface is constitutively exposed to diverse antigens, such as food antigens, food-borne pathogens, and commensal microbes. Intestinal epithelial cells have developed unique barrier functions that prevent the translocation of potentially hostile antigens into the body. Disruption of the epithelial barrier increases intestinal permeability, resulting in leaky gut syndrome (LGS). Clinical reports have suggested that LGS contributes to autoimmune diseases such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and celiac disease. Furthermore, the gut commensal microbiota plays a critical role in regulating host immunity; abnormalities of the microbial community, known as dysbiosis, are observed in patients with autoimmune diseases. However, the pathological links among intestinal dysbiosis, LGS, and autoimmune diseases have not been fully elucidated. This review discusses the current understanding of how commensal microbiota contributes to the pathogenesis of autoimmune diseases by modifying the epithelial barrier.
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