Inflammatory bowel diseases (IBD) are characterized by low proportions of Faecalibacterium prausnitzii in the gut microbiome. F. prausnitzii is a commensal intestinal bacterium known for its anti-inflammatory activity, although its mechanisms of action are still unknown.
In a recent paper published in mBio, a team of INRA researchers proposed clues on how this anti-inflammatory effect is mediated in a gnobiotic mouse model of acute colitis. The study revealed the positive effects of F. prausnitzii on inflammation.
An E. coli and F. prausnitzii-diassociated mouse model was subjected to 2,4,6-trinitrobenzenesulfonic acid (TNBS), a component that induces ulcerative colitis in the large intestine and colon in order to model IBD. The potential anti-inflammatory metabolites were tested in vitro and in vivo. In this model, the researchers observed that F. prausnitzii showed protective effects, observed locally in the colon, associated with a specific metabolite profile along the gastro-intestinal tract and in the serum, such as a-ketoglutarate, raffinose and the anti-inflammatory shikimic and salicylic acids; and a functional link was established in vitro for salicylic acid. The authors showed that F. prausnitzii is a highly active commensal bacterium involved in reduction of colitis through in vivo modulation of metabolites along the gastrointestinal tract and in the peripheral blood.
This work paves the way for further research targeting F. prausnitzii metabolic pathways as a therapeutic approach in IBD.