Insights into Roseburia intestinalis which alleviates experimental colitis pathology by inducing anti-inflammatory responses.

Abstract

The study aims to elucidate the anti-inflammatory effect and mechanism of Roseburia intestinalis (R.intestinalis) in Crohn's disease (CD). 16S-rRNA genome sequencing technique is used to detect the characteristics of intestinal microbiota in untreated CD patients and healthy controls. Then the study investigates the effects of R.intestinalis on disease activity index score, intestinal pathology, the differentiation of Treg cells, and the expressions of Thymic stromal lymphopoietin (TSLP), TGF-β and IL-10 by using TNBS colitis models. At the cellular level, the study uses LPS to stimulate Caco-2 cells to conduct inflammation models and then co-culture with R.intestinalis and detect changes of TSLP and TGF-β. The study then uses R.intestinalis to stimulate peripheral blood mononuclear cells, and the change of Treg cells was detected. Genome sequencing of fecal samples from untreated CD patients (n=10) revealed decreases in the abundance and diversity of intestinal microbiota, including R.intestinalis. Moreover, R.intestinalis reduced disease activity index scores, colon shortening, intestinal mucosal epithelial injury, and mucosal lymphocyte infiltration in a colitis mice model. It suppressed intestinal inflammation by increasing Treg cell numbers and expression of the anti-inflammatory cytokines TSLP, TGF-β, and interleukin-10 (P<0.05). R.intestinalis also increased secretion of TSLP and TGF-β in lipopolysaccharide-treated Caco-2 cells. These findings suggest that R.intestinalis suppresses CD pathogenesis by inducing anti-inflammatory responses.