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During bacterial infection, the pathogenic agent and the host battle for iron, due to its importance for fundamental cellular processes. However, iron redistribution and sequestration during infection can culminate in anemia. Although hepcidin has been recognized as the key regulator of iron metabolism, in some infections its levels remain unaffected, suggesting the involvement of other players in iron metabolism deregulation. In this work, we use a mouse model to elucidate the main cellular and molecular mechanisms that lead to iron redistribution during infection with two different pathogens:Listeria monocytogenes andSalmonella enterica serovar Typhimurium. Both infections clearly impacted iron metabolism, causing iron redistribution, decreasing serum iron levels, decreasing the saturation of transferrin, and increasing iron accumulation in the liver. Both infections were accompanied by the release of proinflammatory cytokines. However, when analyzing iron-related gene expression in the liver, we observed that hepcidin was induced byS . Typhimurium but not byL. monocytogenes . In the latter model, the downregulation of hepatic ferroportin mRNA and protein levels suggested that ferroportin plays a major role in iron redistribution. On the other hand,S . Typhimurium infection induced the expression of hepcidin mRNA, and we show here, for the first timein vivo , that this induction is Toll-like receptor 4 (TLR4) dependent. In this work, we compare several aspects of iron metabolism alterations induced by two different pathogens and suggest that hepcidin-(in)dependent mechanisms contribute to iron redistribution upon infection.

Hepcidin-(In)dependent Mechanisms of Iron Metabolism Regulation during Infection by Listeria and Salmonella