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Background and Aims  It has been shown that  Faecalibacterium prausnitzii  ( F. prausnitzii ), one of the dominant intestinal bacterial flora, may protect colonic mucosa against the development of inflammation and subsequent inflammatory bowel disease (IBD), with the underlying mechanisms being unclear.    Methods  The impacts of  F. prausnitzii  and its metabolites on IL-23/Th17/IL-17 pathway markers were determined in human monocytes and a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid.  F. prausnitzii  and its culture medium (containing complete metabolites) were used to treat the rats  in vivo , as well as rat splenocytes and human monocytes  in vitro . Inflammatory cytokines were measured in colon tissue, plasma and cell culture medium.    Results  The culture supernatant of  F. prausnitzii  increased plasma anti-Th17 cytokines (IL-10 and IL-12)and suppressed IL-17 levels in both plasma and colonic mucosa, with ameliorated colonic colitis lesions. This inhibition of IL-17 release has also been observed in both rat splenocytes and human venous monocytes  in vitro . The culture supernatant of  F. prausnitzii  also suppressed Th17 cell differentiation induced by cytokines (TGF-ß and IL-6) and bone marrow-derived dendritic cells (BMDCs)  in vitro . The metabolites of  F. prausnitzii  in the culture supernatant exert a stronger anti-inflammatory effect than the bacterium itself.  F. prausnitzii  protected the colon mucosa against the development of IBD by its metabolites, suggesting a promising potential for the use of  F. prausnitzii  and its metabolic products in the treatment of IBD.

Faecalibacterium prausnitzii Inhibits Interleukin-17 to Ameliorate Colorectal Colitis in Rats