Translocation of a gut pathobiont drives autoimmunity in mice and humans

TLDR

The composition of the commensal microbiota influences autoimmune disease development and persistence. The study identified Enterococcus gallinarum as a gut pathobiont that translocates into organs of lupus‑prone mice, induces gut barrier breakdown and pathogenic T helper cells, and causes reversible pathology with vancomycin or vaccination; the same bacterium was also detected in liver biopsies of autoimmune patients but not healthy controls. Manfredo Vieira et al.

Abstract

Bacterial involvement in autoimmunity The composition of the commensal microbiota is known to influence autoimmune disease development and persistence. Manfredo Vieira et al. identified a gut microbe, Enterococcus gallinarum , that translocates from the gut into the organs of mice with a genetic predisposition to lupus-like autoimmunity (see the Perspective by Citi). Molecular signatures of gut barrier disintegration and pathogenic T helper cells were evident in the gut, liver, and lymphoid organs during colonization with the pathobiont. The ensuing pathology could be reversed by vancomycin treatment and by vaccination against E. gallinarum . The same bug was also found in liver biopsies of autoimmune patients, but not in healthy controls. Science , this issue p. 1156 ; see also p. 1097