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Many years ago, it was postulated that the low serum iron that characterized anemia of chronic disease (now called anemia of inflammation) provided protection from the inflammatory conditions and infections with which it was associated by depriving bacteria of iron on which they were dependent or by removing iron that would otherwise be available for the generation of free radicals.1
The discovery of the iron regulatory peptide hepcidin provided the mechanism by which inflammation, infection, and other cytokine-mediated processes could shift the iron balance from circulation bound to transferrin to intracellular storage in the reticuloendothelial system and could control iron absorption.2 Hepcidin, an element of the innate immune system, is regulated by systemic iron levels, by inflammation, and by the degree of erythroid activity in the bone marrow. This latter effect is mediated principally …
Contributors RTM is the sole author of this work.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests RTM is an Associate Editor for the Journal of Investigative Medicine.
Provenance and peer review Commissioned; externally peer reviewed.