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Retention of iron in tissue macrophages  via  upregulation of hepcidin (HAMP) and downregulation of the iron exporter ferroportin (FPN) is thought to participate in the establishment of anemia of inflammation after infection. However, an upregulation of FPN has been proposed to limit macrophages iron access to intracellular pathogens. Therefore, we studied the iron homeostasis and in particular the regulation of FPN after infection with  Salmonella enterica  serovar Typhimurium in mice presenting tissue macrophages with high iron (AcB61), basal iron (A/J and wild-type mice), or low iron ( Hamp  knock out,  Hamp  −/− ) levels. The presence of iron in AcB61 macrophages due to extravascular hemolysis and strong erythrophagocytosis activity favored the proliferation of  Salmonella  in the spleen and liver with a concomitant decrease of FPN protein expression. Despite systemic iron overload, no or slight increase in  Salmonella  burden was observed in  Hamp  −/−  mice compared to controls. Importantly, FPN expression at both mRNA and protein levels was strongly decreased during  Salmonella  infection in  Hamp  −/−  mice. The repression of  Fpn  mRNA was also observed in  Salmonella -infected cultured macrophages. In addition, the downregulation of FPN was associated with decreased iron stores in both the liver and spleen in infected mice. Our findings show that during  Salmonella  infection, FPN is repressed through an iron and hepcidin-independent mechanism. Such regulation likely provides the cellular iron indispensable for the growth of  Salmonella  inside the macrophages.

Iron- and Hepcidin-Independent Downregulation of the Iron Exporter Ferroportin in Macrophages during Salmonella Infection