Innate lymphoid cells regulate intestinal epithelial cell glycosylation

被引:423
作者
Goto, Yoshiyuki [1 ,2 ,3 ]
Obata, Takashi [1 ,3 ]
Kunisawa, Jun [1 ,4 ,5 ]
Sato, Shintaro [1 ,2 ]
Ivanov, Ivaylo I. [6 ]
Lamichhane, Aayam [1 ]
Takeyama, Natsumi [1 ,7 ]
Kamioka, Mariko [1 ]
Sakamoto, Mitsuo [3 ]
Matsuki, Takahiro [8 ]
Setoyama, Hiromi [8 ]
Imaoka, Akemi [8 ]
Uematsu, Satoshi [9 ,10 ]
Akira, Shizuo [11 ]
Domino, Steven E. [12 ]
Kulig, Paulina [13 ]
Becher, Burkhard [13 ]
Renauld, Jean-Christophe [14 ,15 ]
Sasakawa, Chihiro [7 ,16 ,17 ]
Umesaki, Yoshinori [8 ]
Benno, Yoshimi [18 ]
Kiyono, Hiroshi [1 ,2 ,5 ]
机构
[1] Univ Tokyo, Inst Med Sci, Dept Microbiol & Immunol, Div Mucosal Immunol, Tokyo 1088639, Japan
[2] Japan Sci & Technol Agcy, Core Res Evolut Sci & Technol, Kawaguchi, Saitama 3320012, Japan
[3] RIKEN, BioResource Ctr, Microbe Div Japan Collect Microorganisms, Tsukuba, Ibaraki 3050074, Japan
[4] Natl Inst Biomed Innovat, Lab Vaccine Mat, Osaka 5670085, Japan
[5] Univ Tokyo, Inst Med Sci, Div Mucosal Immunol, Int Res & Dev Ctr Mucosal Vaccines, Tokyo 1088639, Japan
[6] Columbia Univ, Med Ctr, Dept Microbiol & Immunol, New York, NY 10032 USA
[7] Nippon Inst Biol Sci, Tokyo 1980024, Japan
[8] Yakult Cent Inst, Tokyo 1868650, Japan
[9] Univ Tokyo, Inst Med Sci, Int Res & Dev Ctr Mucosal Vaccines, Div Innate Immune Regulat, Tokyo 1088639, Japan
[10] Chiba Univ, Sch Med, Dept Mucosal Immunol, Chuou Ku, Chiba 2608670, Japan
[11] Osaka Univ, WPI Immunol Frontier Res Ctr, Lab Host Def, Osaka 5650871, Japan
[12] Univ Michigan, Med Ctr, Cellular & Mol Biol Program, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA
[13] Univ Zurich, Inst Expt Immunol, CH-8057 Zurich, Switzerland
[14] Ludwig Inst Canc Res, B-1200 Brussels, Belgium
[15] Catholic Univ Louvain, B-1200 Brussels, Belgium
[16] Univ Tokyo, Inst Med Sci, Div Bacterial Infect, Tokyo 1088639, Japan
[17] Chiba Univ, Med Mycol Res Ctr, Chiba 2608673, Japan
[18] RIKEN, Innovat Ctr, Benno Lab, Wako, Saitama 3510198, Japan
基金
日本科学技术振兴机构; 美国国家卫生研究院;
关键词
SEGMENTED FILAMENTOUS BACTERIA; ROR-GAMMA-T; ENTERICA SEROTYPE TYPHIMURIUM; COMMENSAL MICROFLORA; HOST; FUT2; MICROBIOTA; DIFFERENTIATION; SUSCEPTIBILITY; PATHWAY;
D O I
10.1126/science.1254009
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1310 / +
页数:12
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