IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin
Elizabeta Nemeth, … , Bente K. Pedersen, Tomas Ganz
Elizabeta Nemeth, … , Bente K. Pedersen, Tomas Ganz
Published May 1, 2004
Citation Information: J Clin Invest. 2004;113(9):1271-1276. https://doi.org/10.1172/JCI20945.
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Article Hematology

IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin

Abstract

Hypoferremia is a common response to systemic infections or generalized inflammatory disorders. In mouse models, the development of hypoferremia during inflammation requires hepcidin, an iron regulatory peptide hormone produced in the liver, but the inflammatory signals that regulate hepcidin are largely unknown. Our studies in human liver cell cultures, mice, and human volunteers indicate that IL-6 is the necessary and sufficient cytokine for the induction of hepcidin during inflammation and that the IL-6–hepcidin axis is responsible for the hypoferremia of inflammation.

Authors

Elizabeta Nemeth, Seth Rivera, Victoria Gabayan, Charlotte Keller, Sarah Taudorf, Bente K. Pedersen, Tomas Ganz

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Counterregulation of hepcidin mRNA expression by TNF-α. Human hepatoma H...
Counterregulation of hepcidin mRNA expression by TNF-α. Human hepatoma Hep3B cells were treated with 20 ng/ml of the indicated cytokine(s) with or without anti_IL-6 Ab's for 24 hours. Their hepcidin mRNA was then analyzed relative to G3PDH mRNA by qRT-PCR. In each experiment, the hepcidin mRNA was expressed as a ratio to that of untreated cells (0), and the mean and standard deviation of four experiments are shown. Paired Student's t test was used to determine the significance of the effects of TNF-α.