Abstract
Hepcidin is presumed to be the principal mediator of anemia of inflammation (AI) and anemia of cancer (AC). Hepcidin is elevated in these conditions and an inducible hepcidin overexpressing mouse develops a clinical syndrome nearly identical to AI (Roy et al, Blood, 2007). However, no study has determined whether hepcidin is necessary for the development of AI and AC. Using mouse models of AC and AI in hepcidin knockout mice (KO) and wild type controls (WT), we sought to determine whether hepcidin was necessary for the development of anemia in these conditions. In AI, hemoglobin fell to a much lesser extent in KO mice. In AC, hemoglobin fell to a similar degree in WT and KO mice. However, in AC the tumor produced some hepcidin. KO mice have polycythemia at baseline so they are much less anemic than WT mice even in the presence of inflammation and cancer. Hepcidin plays an important role in AI and AC. Future studies will determine whether antagonism of hepcidin after the onset of disease will treat these conditions.
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