<i>Ruminococcus gnavus</i>is a pathobiont expanded by genetic susceptibility and dietary tryptophan in a lupus-prone mouse model

Abstract Gut microbial dysbiosis has been associated with the development of systemic lupus erythematosus (SLE). Dietary tryptophan modifies composition gut microbiota as well disease activity in a lupus-prone mouse (TC). To directly test modulatory function on microbiota, we transplanted from TC and B6 control mice into germ-free or antibiotic treated recipients fed high low dietary tryptophan. Interestingly, putative human pathobiont Ruminococcus gnavus (Rg) was only enriched tryptophan, which produced anti-dsDNA IgA presented T cell infiltration kidney. A higher level Rg detected untouched compared to controls, correlation levels signature cytokines. Depletion this bacterium decreased autoantibody production increased frequency regulatory cells. Conversely, monocolonization antibiotic-treated induced IFN-γ+ cells, IL-10+ non-T cells GC B age-matched mice. These results indicate that is sufficient induce autoimmune activation model expanded by combination genetic susceptibility This project supported grant RO1 AI143313 NIH LMo.