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Get Free AccessFucosylation 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.
Yoshiyuki Goto, Takashi Obata, Jun Kunisawa, Shintaro Sato, Ivaylo I. Ivanov, Aayam Lamichhane, Natsumi Takeyama, Mariko Kamioka, Mitsuo Sakamoto, Takahiro Matsuki, Hiromi Setoyama, Akemi Imaoka, Satoshi Uematsu, Akira Shizuo, Steven E. Domino, Paulina Kulig, Burkhard Becher, Jean‐Christophe Renauld, Chihiro Sasakawa, Yoshinori Umesaki, Yoshimi Benno, Hiroshi Kiyono (2014). Innate lymphoid cells regulate intestinal epithelial cell glycosylation. Science, 345(6202), DOI: 10.1126/science.1254009.
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Type
Article
Year
2014
Authors
22
Datasets
0
Total Files
0
Language
English
Journal
Science
DOI
10.1126/science.1254009
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