Inhibition of Aryl hydrocarbon receptor Interleukin-22 signaling and worsening of intestinal inflammation by Sutterella species.

چکیده اصلی

The gut microbiota constitutes a complex ecosystem essential for host defense against infection and immune system maturation. Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, are characterized by a severe inflammation of the intestine, arising from dysregulated control of host-microbiota crosstalk. However, neither the genetic bases of IBD nor the immune responses involved are fully understood. Pathobionts are currently under investigation for their active role in the development and severity of IBD. These bacteria are present in the gut microbiota of healthy individuals without causing disease, but have pathogenic potential when the intestinal environment is disturbed. Here, we highlight Sutterella sp. as a new commensal pathobiont for its capacity to modulate the host's immune functions. This anaerobic Gram-negative bacterium inhibits the production of IL-22 and IL-17 by lymphoid cells, ex vivo and in vivo. In the DSS-colitis model, Sutterella sp. can increase intestinal inflammation and inhibit IL-22 production. Moreover, the production of IL-22 and IL-17 by human lymphoid cells is also reduced by Sutterella sp. The bacterium acts directly on lymphoid cells through the secretion of protein-based compounds that antagonize AhR signaling. These data enhance our understanding of the mechanisms that regulate host immune functions and pave the way for new therapeutic strategies to control gut inflammation.

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