Hepcidin and the Iron-Infection Axis
Editorial: science
Fecha: 01/11/2012
Hal Drakesmith1* and Andrew M. Prentice2*
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.
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.