AI Article Synopsis

  • Intestinal inflammation alters the composition and metabolism of gut microbiota, but the host's response to these changes is not fully understood.* -
  • Mucosal-associated invariant T (MAIT) cells can detect metabolites from riboflavin-producing bacteria that increase during inflammation, promoting tissue repair in the intestines.* -
  • Mice without MAIT cells showed higher susceptibility to colitis and related colorectal cancer, highlighting the significance of MAIT cells in responding to gut inflammation through bacterial metabolic pathways.*

Article Abstract

Intestinal inflammation shifts microbiota composition and metabolism. How the host monitors and responds to such changes remains unclear. Here, we describe a protective mechanism by which mucosal-associated invariant T (MAIT) cells detect microbiota metabolites produced upon intestinal inflammation and promote tissue repair. At steady state, MAIT ligands derived from the riboflavin biosynthesis pathway were produced by aerotolerant bacteria residing in the colonic mucosa. Experimental colitis triggered luminal expansion of riboflavin-producing bacteria, leading to increased production of MAIT ligands. Modulation of intestinal oxygen levels suggested a role for oxygen in inducing MAIT ligand production. MAIT ligands produced in the colon rapidly crossed the intestinal barrier and activated MAIT cells, which expressed tissue-repair genes and produced barrier-promoting mediators during colitis. Mice lacking MAIT cells were more susceptible to colitis and colitis-driven colorectal cancer. Thus, MAIT cells are sensitive to a bacterial metabolic pathway indicative of intestinal inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7616241PMC
http://dx.doi.org/10.1126/sciimmunol.adi8954DOI Listing

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