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 Blood, 15 February 2008, Vol. 111, No. 4, pp. 2392-2399.
Prepublished online as a Blood First Edition Paper on December 11, 2007; DOI 10.1182/blood-2007-05-090019.

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PHAGOCYTES

Autocrine formation of hepcidin induces iron retention in human monocytes

Igor Theurl1, Milan Theurl1, Markus Seifert1, Sabine Mair1, Manfred Nairz1, Holger Rumpold2, Heinz Zoller3, Rosa Bellmann-Weiler1, Harald Niederegger4, Heribert Talasz5, and Günter Weiss1

Departments of1 General Internal Medicine, 2 Hematology and Oncology, and 3 Gastroenterology and Hepatology, Medical University, Innsbruck; 4 Tyrolean Cancer Research Institute, Innsbruck; and 5 Biocenter, Division of Clinical Biochemistry, Medical University, Innsbruck, Austria

Hepcidin, a master regulator of iron homeostasis, is produced in small amounts by inflammatory monocytes/macrophages. Chronic immune activation leads to iron retention within monocytes/macrophages and the development of anemia of chronic disease (ACD). We questioned whether monocyte-derived hepcidin exerts autocrine regulation toward cellular iron metabolism. Monocyte hepcidin mRNA expression was significantly induced within 3 hours after stimulation with LPS or IL-6, and hepcidin mRNA expression was significantly higher in monocytes of ACD patients than in controls. In ACD patients, monocyte hepcidin mRNA levels were significantly correlated to serum IL-6 concentrations, and increased monocyte hepcidin mRNA levels were associated with decreased expression of the iron exporter ferroportin and iron retention in these cells. Transient transfection experiments using a ferroportin/EmGFP fusion protein construct demonstrated that LPS inducible hepcidin expression in THP-1 monocytes resulted in internalization and degradation of ferroportin. Transfection of monocytes with siRNA directed against hepcidin almost fully reversed this lipopolysaccharide-mediated effect. Using ferroportin mutation constructs, we found that ferroportin is mainly targeted by hepcidin when expressed on the cell surface. Our results suggest that ferroportin expression in inflammatory monocytes is negatively affected by autocrine formation of hepcidin, thus contributing to iron sequestration within monocytes as found in ACD.


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