We are investigating how iron and anaemia influence immunity and infectious diseases. Our research inspires treatments that control iron physiology to benefit the host at the expense of pathogens.
Iron is critical for life: too little can halt DNA synthesis and energy metabolism; too much can generate toxic reactive oxygen species. Furthermore, iron is essential for the growth of pathogens, but also for the immune system that fights infections. For example, during infection the host sequesters iron to deprive pathogens as part of the innate immune response, while T cells and B cells need iron for their function to clear the infection.
Iron levels in the body are controlled by a hormone called hepcidin, which acts analogously to how insulin controls glucose. Through collaborators in Europe, the US, Africa and Sri Lanka we have made significant contributions to how hepcidin and iron are controlled in health and disease, including anaemia, HIV, HCV and typhoid fever. We utilise experimental models of key diseases, including malaria, to manipulate hepcidin during infection and understand how iron affects immunity and the outcome of infection.
Clinical Studies and Trials
Iron deficiency anaemia affects one sixth of the world’s population and has a variety of causes including low levels of dietary iron or chronic inflammation limiting iron availability. In cases where iron deficiency is the result of an infection, iron supplementation can enhance pathogen growth with lethal consequences. Our lab has pioneered new approaches to identify the “type” of iron deficiency anaemia and therefore the appropriate treatment option. These approaches are being trialled in Africa and in Oxford.
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