期刊
SCIENCE
卷 368, 期 6487, 页码 186-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aau6481
关键词
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资金
- Crohn's and Colitis Foundation fellowship [F32AI124517]
- NIH
- MAID Mucosal Immunology Studies Team (MIST) [R0IAI143842, R0IAI123368, R0IAI145989, R21CA249274, U0IAI095608]
- Searle Scholars Program
- American Asthma Foundation Scholar Award
- Burroughs Wellcome Fund
- Wade F. B. Thompson/Cancer Research Institute (CRI) CLIP Investigator grant
- Meyer Cancer Center Collaborative Research Initiative
- CRI Lloyd J. Old STAR
- European Research Council [261296]
- Fondation pour la Recherche Madicale
- Laboratory of Excellence GR-Ex [20160334903]
- labex GR-Ex fellowship [ANR-11-LABX-O051]
- French National Research Agency [ANR-11-IDEX-0005-02]
- Science Foundation Ireland [PP30ES023515, 1U2CES030859, ROOHL125899, ROOHD087523]
- Cure for IBD [FRL4862 (S.MC)]
- Rosanne H. Silbermann Foundation
- Weill Cornell Medicine Division of Pediatric Gastroenterology and Nutrition
- European Research Council (ERC) [261296] Funding Source: European Research Council (ERC)
Bleeding and altered iron distribution occur in multiple gastrointestinal diseases, but the importance and regulation of these changes remain unclear. We found that hepcidin, the master regulator of systemic iron homeostasis, is required for tissue repair in the mouse intestine after experimental damage. This effect was independent of hepatocyte-derived hepcidin or systemic iron levels. Rather, we identified conventional dendritic cells (cDCs) as a source of hepcidin that is induced by microbial stimulation in mice, prominent in the inflamed intestine of humans, and essential for tissue repair. cDC-derived hepcidin acted on ferroportin-expressing phagocytes to promote local iron sequestration, which regulated the microbiota and consequently facilitated intestinal repair. Collectively, these results identify a pathway whereby cDC-derived hepcidin promotes mucosal healing in the intestine through means of nutritional immunity.
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