In the steady state, iron levels in the plasma are regu- lated by the recycling of iron from senescent red blood cells by macrophages of the reticuloendothelial sys- tem. In systemic infections and inflammatory states, per- turbation of this process can result in hypoferremia (a decrease in circulating iron levels), which may represent a host defense mechanism to limit iron availability to pathogens. 1 Because hypoferremia restricts the availabili- ty of iron to erythroid precursors, if sustained, it con- tributes to the development of the anemia of inflamma- tion. In this issue of Haematologica, Agoro et al. 2 report that the acute hypoferremic response to lipopolysaccha- ride (LPS), a major component of the outer membrane of Gram-negative bacteria, is modulated in mice by pre- treatment with a truncated, C-terminal fragment of the hormone fibroblast growth factor 23.
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