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Almost all forms of life require iron to thrive. Iron plays essential biochemical roles in oxygen binding, ATP synthesis and DNA metabolism. During infection, pathogens need to acquire iron from their human host. If iron availability is high, infections can progress more rapidly. On the other hand, denying iron to invading microbes can slow down the course of disease, and allow immune mechanisms more time to clear the infection. Pathogens can become resistant to antibiotics, and can sometimes mutate to avoid recognition by the immune systems, but they cannot escape the metabolic requirement for iron. By manipulating iron transport we hope to develop a new strategy to combat infections.
The human peptide hepcidin is the master controller of iron metabolism; too little hepcidin leads to iron overload, too much causes anaemia. We are defining how hepcidin is modulated during infections, by testing which aspects of pathogen recognition by the host influence hepcidin synthesis. We then will assess whether deliberately altering hepcidin can control experimental infections of iron-requiring bacterial strains.
The human peptide hepcidin is the master controller of iron metabolism; too little hepcidin leads to iron overload, too much causes anaemia. We are defining how hepcidin is modulated during infections, by testing which aspects of pathogen recognition by the host influence hepcidin synthesis. We then will assess whether deliberately altering hepcidin can control experimental infections of iron-requiring bacterial strains.
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CELL HOST & MICROBEno. 1 (2024): 1-2
Advances in Nutritionpp.100238-100238, (2024)
Cell Host & Microbeno. 1 (2024): 1-2
Lilac Tene, Avraham Karasik,Gabriel Chodick, Dora I A Pereira, Henrik Schou, Sandra Waechter, Udo-Michael Göhring,Hal Drakesmith
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bioRxiv : the preprint server for biology (2023)
The Lancet. Global healthno. 1 (2023): e105-e116
ANNALS OF NUTRITION AND METABOLISM (2023): 422-422
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International journal of obesity (2005)no. 7 (2023): 554-563
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