期刊
MUCOSAL IMMUNOLOGY
卷 11, 期 3, 页码 763-773出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2017.86
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资金
- Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries and Food Industry
- CREST
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Grants-in-Aid for Scientific Research [15H05787] Funding Source: KAKEN
Dectin-1 (gene symbol: Clec7a) is a receptor for beta-glucans that play an important role for the host defense against fungi. Recently, we showed that Clec7a(-/-) mice are resistant against dextran sodium sulfate (DSS)-induced colitis because of regulatory T-cell population expansion in the colon. The regulatory T-cell expansion is caused by expansion of commensal Lactobacillus murinus whose growth is suppressed by an antimicrobial protein, calprotectin S100A8/A9. In this report, we showed that S100A8 was mainly produced by mouse colonic epithelial cells. S100A8 was not induced directly by Dectin-1 but by Dectin-1-induced cytokines, especially interleukin-17F (IL-17F), that were produced by several types of innate immune cells including CD11c(+)/CD11b(+) myeloid cells in colonic lamina propria. S100A8/A9 heterodimer preferentially suppressed the growth of L. murinus that was increased in both Clec7a(-/-) and II17f(-/-) mice. Furthermore, similar expansion of L. murinus and DSS-colitis resistance were observed in mice fed with beta-glucanfree food. These observations suggest that food-derived b-glucans control the specific commensal microbiota via the Dectin-1-IL-17F-calprotectin axis to maintain the intestinal homeostasis.
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