Hepcidin and the Iron-Infection Axis

被引:579
作者
Drakesmith, Hal [1 ,2 ]
Prentice, Andrew M. [3 ]
机构
[1] Univ Oxford, John Radcliffe Hosp, Mol Immunol Grp, Oxford OX3 9DS, England
[2] Univ Oxford, John Radcliffe Hosp, Med Res Council MRC, Human Immunol Unit,MRC Weatherall Inst Mol Med, Oxford OX3 9DS, England
[3] Univ London London Sch Hyg & Trop Med, MRC Int Nutr Grp, London WC1E 7HT, England
基金
英国医学研究理事会;
关键词
PATHOGEN INTERACTIONS; PEPTIDE HEPCIDIN; FERROPORTIN; GENE; MALARIA; ANEMIA; SUSCEPTIBILITY; SALMONELLA; OVERLOAD; HOST;
D O I
10.1126/science.1224577
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
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
Iron lies at the center of a battle for nutritional resource between higher organisms and their microbial pathogens. The iron status of the human host affects the pathogenicity of numerous infections including malaria, HIV-1, and tuberculosis. Hepcidin, an antimicrobial-like peptide hormone, has emerged as the master regulator of iron metabolism. Hepcidin controls the absorption of dietary iron and the distribution of iron among cell types in the body, and its synthesis is regulated by both iron and innate immunity. We describe how hepcidin integrates signals from diverse physiological inputs, forming a key molecular bridge between iron trafficking and response to infection.
引用
收藏
页码:768 / 772
页数:5
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