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环境暴露与自身免疫性疾病:肠道微生物组的作用。

Environmental Exposures and Autoimmune Diseases: Contribution of Gut Microbiome.

机构信息

Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, TX, United States.

出版信息

Front Immunol. 2020 Jan 10;10:3094. doi: 10.3389/fimmu.2019.03094. eCollection 2019.

DOI:10.3389/fimmu.2019.03094
PMID:31998327
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6970196/
Abstract

Environmental agents have been gaining more attention in recent years for their role in the pathogenesis of autoimmune diseases (ADs). Increasing evidence has linked environmental exposures, including trichloroethene (TCE), silica, mercury, pristane, pesticides, and smoking to higher risk for ADs. However, potential mechanisms by which these environmental agents contribute to the disease pathogenesis remains largely unknown. Dysbiosis of the gut microbiome is another important environmental factor that has been linked to the onset of different ADs. Altered microbiota composition is associated with impaired intestinal barrier function and dysregulation of mucosal immune system, but it is unclear if gut dysbiosis is a causal factor or an outcome of ADs. In this review article, we first describe the recent epidemiological and mechanistic evidences linking environmental/occupational exposures with various ADs (especially SLE). Secondly, we discuss how changes in the gut microbiome composition (dysbiosis) could contribute to the disease pathogenesis, especially in response to exposure to environmental chemicals.

摘要

近年来,环境因素在自身免疫性疾病(AD)发病机制中的作用越来越受到关注。越来越多的证据表明,环境暴露,包括三氯乙烯(TCE)、二氧化硅、汞、降植烷、农药和吸烟,与 AD 的更高风险相关。然而,这些环境因素导致疾病发病机制的潜在机制在很大程度上尚不清楚。肠道微生物组的失调是另一个与不同 AD 发病相关的重要环境因素。微生物组成的改变与肠道屏障功能受损和黏膜免疫系统失调有关,但尚不清楚肠道菌群失调是 AD 的因果因素还是结果。在这篇综述文章中,我们首先描述了将环境/职业暴露与各种 AD(尤其是 SLE)联系起来的最新流行病学和机制证据。其次,我们讨论了肠道微生物组组成的变化(失调)如何有助于疾病发病机制,特别是对环境化学物质暴露的反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac57/6970196/91f22bd6f5a8/fimmu-10-03094-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac57/6970196/edef780c244e/fimmu-10-03094-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac57/6970196/91f22bd6f5a8/fimmu-10-03094-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac57/6970196/edef780c244e/fimmu-10-03094-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac57/6970196/91f22bd6f5a8/fimmu-10-03094-g0002.jpg

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