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. 2019 Jun 6;10:615. doi: 10.3389/fphar.2019.00615

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Copyright © 2019 Scindia, Wlazlo, Leeds, Loi, Ledesma, Cechova, Ghias and Swaminathan

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism depicting hepcidin’s protective effect in settings of endotoxemia and live infections. Endotoxemia and live infections cause a rapid, systematic activation of immune cells, including macrophages, which secrete cytokines like TNFα, IL-6 and IL-1β. This toxic milieu initiates SIRS and eventually worsens AKI. Hepcidin pretreatment attenuates macrophage inflammatory response to endotoxin. In parallel, by sequestering iron within tissue (mostly macrophages), hepcidin limits iron availability, a key nutrient for invading pathogens and thereby reduces bacterial load. Thus, hepcidin limits AKI by dual mechanisms: 1) by reducing macrophage inflammatory response and reducing overall serum cytotoxicity, and 2) by reducing pathogen load.