Infectivology and Clinical Trials Research Department, Children's Hospital Bambino Gesù, Viale San Paolo 15, 00146 Rome, Italy.
VisMederi s.r.l., Strada del Petriccio e Belriguardo, 35, 53100 Siena, Italy.
Int J Mol Sci. 2019 Jan 11;20(2):283. doi: 10.3390/ijms20020283.
Autoimmune disorders derive from genetic, stochastic, and environmental factors that all together interact in genetically predisposed individuals. The impact of an imbalanced gut microbiome in the pathogenesis of autoimmunity has been suggested by an increasing amount of experimental evidence, both in animal models and humans. Several physiological mechanisms, including the establishment of immune homeostasis, are influenced by commensal microbiota in the gut. An altered microbiota composition produces effects in the gut immune system, including defective tolerance to food antigens, intestinal inflammation, and enhanced gut permeability. In particular, early findings reported differences in the intestinal microbiome of subjects affected by several autoimmune conditions, including prediabetes or overt disease compared to healthy individuals. The present review focuses on microbiota-host homeostasis, its alterations, factors that influence its composition, and putative involvement in the development of autoimmune disorders. In the light of the existing literature, future studies are necessary to clarify the role played by microbiota modifications in the processes that cause enhanced gut permeability and molecular mechanisms responsible for autoimmunity onset.
自身免疫性疾病源于遗传、随机和环境因素，这些因素共同作用于具有遗传易感性的个体。越来越多的实验证据表明，肠道微生物组失衡在自身免疫的发病机制中起作用，无论是在动物模型还是人类中。一些生理机制，包括免疫稳态的建立，都受到肠道共生微生物的影响。微生物群落组成的改变会对肠道免疫系统产生影响，包括对食物抗原的耐受性缺陷、肠道炎症和肠道通透性增强。特别是，早期的研究结果报告了几种自身免疫性疾病患者的肠道微生物组存在差异，包括前驱糖尿病或显性疾病与健康个体相比存在差异。本综述重点介绍了微生物群-宿主的稳态、其改变、影响其组成的因素以及在自身免疫性疾病发展中的潜在作用。根据现有文献，需要进一步研究来阐明微生物组改变在增强肠道通透性的过程中以及负责自身免疫发病机制的分子机制中所起的作用。
