Translocation of a gut pathobiont drives autoimmunity in mice and humans. | Read by QxMD (original) (raw)
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
S Manfredo Vieira, M Hiltensperger, V Kumar, D Zegarra-Ruiz, C Dehner, N Khan, F R C Costa, E Tiniakou, T Greiling, W Ruff, A Barbieri, C Kriegel, S S Mehta, J R Knight, D Jain, A L Goodman, M A Kriegel
Despite multiple associations between the microbiota and immune diseases, their role in autoimmunity is poorly understood. We found that translocation of a gut pathobiont, Enterococcus gallinarum , to the liver and other systemic tissues triggers autoimmune responses in a genetic background predisposing to autoimmunity. Antibiotic treatment prevented mortality in this model, suppressed growth of E. gallinarum in tissues, and eliminated pathogenic autoantibodies and T cells. Hepatocyte- E. gallinarum cocultures induced autoimmune-promoting factors. Pathobiont translocation in monocolonized and autoimmune-prone mice induced autoantibodies and caused mortality, which could be prevented by an intramuscular vaccine targeting the pathobiont. E. gallinarum -specific DNA was recovered from liver biopsies of autoimmune patients, and cocultures with human hepatocytes replicated the murine findings; hence, similar processes apparently occur in susceptible humans. These discoveries show that a gut pathobiont can translocate and promote autoimmunity in genetically predisposed hosts.
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