Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA.
Department of Medicine, Yale School of Medicine, New Haven, CT, USA.
Gut Microbes. 2020;11(2):217-230. doi: 10.1080/19490976.2019.1629236. Epub 2019 Jul 15.
Humans and other mammalian hosts have evolved mechanisms to control the bacteria colonizing their mucosal barriers to prevent invasion. While the breach of barriers by bacteria typically leads to overt infection, increasing evidence supports a role for translocation of commensal bacteria across an impaired gut barrier to extraintestinal sites in the pathogenesis of autoimmune and other chronic, non-infectious diseases. Whether gut commensal translocation is a cause or consequence of the disease is incompletely defined. Here we discuss factors that lead to translocation of live bacteria across the gut barrier. We expand upon our recently published demonstration that translocation of the gut pathobiont can induce autoimmunity in susceptible hosts and postulate on the role of species as instigators of chronic, non-infectious diseases.
人类和其他哺乳动物宿主已经进化出控制定植在其黏膜屏障上的细菌的机制,以防止细菌入侵。虽然细菌突破屏障通常会导致明显的感染,但越来越多的证据支持共生菌通过受损的肠道屏障易位到肠道外部位在自身免疫和其他慢性非传染性疾病的发病机制中的作用。肠道共生菌易位是疾病的原因还是结果尚不完全清楚。在这里,我们讨论导致活细菌穿过肠道屏障易位的因素。我们扩展了我们最近发表的研究,证明肠道条件致病菌的易位可以在易感宿主中诱导自身免疫,并推测 物种作为慢性非传染性疾病的引发因素的作用。