Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan. Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan.
Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan.
Science. 2014 Sep 12;345(6202):1254009. doi: 10.1126/science.1254009. Epub 2014 Aug 21.
Fucosylation of intestinal epithelial cells, catalyzed by fucosyltransferase 2 (Fut2), is a major glycosylation mechanism of host-microbiota symbiosis. Commensal bacteria induce epithelial fucosylation, and epithelial fucose is used as a dietary carbohydrate by many of these bacteria. However, the molecular and cellular mechanisms that regulate the induction of epithelial fucosylation are unknown. Here, we show that type 3 innate lymphoid cells (ILC3) induced intestinal epithelial Fut2 expression and fucosylation in mice. This induction required the cytokines interleukin-22 and lymphotoxin in a commensal bacteria-dependent and -independent manner, respectively. Disruption of intestinal fucosylation led to increased susceptibility to infection by Salmonella typhimurium. Our data reveal a role for ILC3 in shaping the gut microenvironment through the regulation of epithelial glycosylation.
肠道上皮细胞的岩藻糖化作用，由岩藻糖基转移酶 2（Fut2）催化，是宿主-微生物共生的主要糖基化机制。共生菌诱导上皮细胞的岩藻糖化，而上皮细胞的岩藻糖被许多这些细菌用作膳食碳水化合物。然而，调节上皮细胞岩藻糖化诱导的分子和细胞机制尚不清楚。在这里，我们表明，3 型固有淋巴细胞（ILC3）在小鼠中诱导肠道上皮 Fut2 表达和岩藻糖化。这种诱导分别需要细胞因子白细胞介素 22 和淋巴毒素，且依赖于共生菌。肠道岩藻糖基化的破坏导致对鼠伤寒沙门氏菌感染的易感性增加。我们的数据揭示了 ILC3 通过调节上皮细胞糖基化在塑造肠道微环境中的作用。
