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.

中文翻译：

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MAIT 细胞监测肠道生态失调并有助于结肠炎期间的宿主保护


肠道炎症会改变微生物群的组成和代谢。宿主如何监控和应对此类变化仍不清楚。在这里，我们描述了一种保护机制，通过该机制，粘膜相关不变 T (MAIT) 细胞可以检测肠道炎症产生的微生物代谢物并促进组织修复。在稳定状态下，源自核黄素生物合成途径的 MAIT 配体由结肠粘膜中的耐氧细菌产生。实验性结肠炎引发核黄素产生细菌的管腔扩张，导致 MAIT 配体的产生增加。肠道氧水平的调节表明氧在诱导 MAIT 配体产生中发挥作用。结肠中产生的 MAIT 配体快速穿过肠屏障并激活 MAIT 细胞，这些细胞在结肠炎期间表达组织修复基因并产生屏障促进介质。缺乏 MAIT 细胞的小鼠更容易患结肠炎和结肠炎引起的结直肠癌。因此，MAIT 细胞对指示肠道炎症的细菌代谢途径敏感。