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IL-22 controls transmissible colitis

机译：IL-22控制传染性结肠炎

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IL-22 is an important cytoldne at barrier surfaces that triggers the production of antimicrobial peptides and mucus. Flavell and colleagues in the Journal of Immunology use an IL-22-deficient mouse to demonstrate that this cytoldne shapes the population of colonic microbes to prevent colitogenicity. IL-22-deficient mice have ostensibly normal colonic morphology and do not manifest spontaneous inflammation; however, induced colitis is worse in those mice than in wild-type mice. Furthermore, wild-type mice cohoused with IL-22-deficient mice have more severe induced colitis, which suggests that the colitis is transmissible. Pyrosequencing indicates that the microbial phyla in IL-22-deficient mice differs from that of wild-type mice and, more notably, the micro-biota of wild-type mice cohoused with IL-22-deficient mice more closely resembles that of the IL-22-deficient mice. As expected, IL-22-deficient mice have a lower abundance of the antimicrobial peptides Reglllp and Regllly but, curiously, so do wild-type mice cohoused with those mice. This suggests that the microbiota is both shaped by IL-22 and, in turn, also influences its expression.
机译：IL-22是在屏障表面上重要的细胞因子，可触发抗菌肽和粘液的产生。 Flavell及其同事在《免疫学杂志》（Journal of Immunology）上使用了一种IL-22缺陷型小鼠来证明这种细胞因子可以塑造结肠微生物的种群，从而防止致细菌性。 IL-22缺陷的小鼠表面上看似正常的结肠形态，没有表现出自发炎症。但是，与野生型小鼠相比，这些小鼠的诱发性结肠炎更为严重。此外，与IL-22缺陷型小鼠共存的野生型小鼠具有更严重的诱导性结肠炎，这表明该结肠炎是可传播的。焦磷酸测序表明，IL-22缺陷型小鼠中的微生物菌群与野生型小鼠不同，更值得注意的是，与IL-22缺陷型小鼠共存的野生型小鼠的微生物群与IL相似-22缺陷小鼠。正如预期的那样，IL-22缺陷型小鼠的抗菌肽Reglllp和Regllly的丰度较低，但是奇怪的是，与这些小鼠共居的野生型小鼠也是如此。这表明微生物群既受IL-22的影响，又会影响其表达。

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