Translocation of a gut pathobiont drives autoimmunity in mice and humans, 2018, Kriegel et al

Andy

Senior Member (Voting rights)
Abstract
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.
Paywalled at http://science.sciencemag.org/content/359/6380/1156

Article about the study
https://news.yale.edu/2018/03/08/enemy-within-gut-bacteria-drive-autoimmune-disease
 
A recent Yale article seems to be an update of Kriegel's work.

Small Steps Lead to Big Results
April 3, 2018
https://medicine.yale.edu/whr/news/article.aspx?id=17076
“Yale" said:
The next step is to bring this work to humans,” Kriegel said. “It’s a natural progression from what I’ve done so far.”

Kriegel’s most promising current avenue of inquiry began in 2013 with a seed grant from Women’s Health Research at Yale and an educated hunch about the outsized role played by one of the tiny organisms that live in our bodies and make up what is called the microbiome.

Kriegel demonstrated how one of the beneficial bacteria that live in our gut might trick the body into developing antiphospholipid syndrome (APS), an autoimmune reaction more common in women.
 
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