Mechanisms and consequences of gut commensal translocation in chronic diseases

Gut Microbes. 2020;11(2):217-230. doi: 10.1080/19490976.2019.1629236. Epub 2019 Jul 15.

Abstract

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 Enterococcus gallinarum can induce autoimmunity in susceptible hosts and postulate on the role of Enterococcus species as instigators of chronic, non-infectious diseases.

Keywords: Gut vascular barrier; TLR7; autoimmune liver disease; autoimmunity; bacterial translocation; enterococcus; gut lymphatic barrier; intestinal permeability; lupus; microbiota; tight junctions; vancomycin resistance.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases* / immunology
  • Autoimmune Diseases* / microbiology
  • Autoimmunity
  • Bacteria / immunology
  • Bacterial Translocation / immunology*
  • Chronic Disease
  • Enterococcus / immunology
  • Enterococcus / pathogenicity
  • Gastrointestinal Microbiome / immunology
  • Humans
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / microbiology*
  • Microbiota / immunology
  • Symbiosis

Supplementary concepts

  • Enterococcus gallinarum