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. Author manuscript; available in PMC: 2015 May 14.
Published in final edited form as: Cell Host Microbe. 2014 May 14;15(5):515–516. doi: 10.1016/j.chom.2014.04.012

Figure 1. Estrogen-Related Receptor γregulates host iron trafficking by inducing hepcidin formation in the liver.

Figure 1

ERRγ transcription is stimulated by interleukin-6 (IL-6) and the transcription factor STAT3. Hepcidin is released into the circulation and binds to the iron export protein ferroportin 1 (FP1), resulting in FP1 degradation and macrophage iron retention. This results in systemic hypoferremia butincreases access of the intracellular pathogen Salmonella to iron. The increase in macrophage iron levels alsoinhibitsinterferon-γ-dependent anti-bacterial immune responses. ERRγinhibition by the reverse agonist GSK5182 counteracts the effects of hepcidin on intra-macrophage iron availability and anti-microbial immune effector pathways but may increase the availability of iron to extracellular pathogens.