Hepcidin, Iron and Infections
|ING Staff:||Andrew Prentice, Rita Wegmüller, Amat Bah, Hans Verhoef|
Iron lies at the centre of the host-pathogen battle for nutritional resources. Micro-organisms have evolved a wide array of mechanisms for sequestering iron; for instance there are over 500 known bacterial siderophores. In opposition to these the human host has evolved a suite of chaperone proteins, and systems to regulate their production, in order to deprive pathogens of iron.
Hepcidin is the master regulator of iron metabolism and integrates signals from iron deficiency/surplus and from infectious threats. Recent proof-of-principle studies in malaria have shown that the iron-hepcidin axis constitutes a newly discovered arm of innate immunity.
In collaboration with several groups, especially Hal Drakesmith and his team at the Weatherall Institute of Molecular Medicine in Oxford, we have recently formed a consortium to coordinate a range of studies on hepcidin, iron and infection with emphasis on HIV, TB and malaria. We are also developing point-of-care tests for iron deficiency based upon hepcidin.