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Originally published In Press as doi:10.1074/jbc.M209768200 on October 23, 2002

J. Biol. Chem., Vol. 277, Issue 51, 49727-49734, December 20, 2002
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Intraphagosomal Mycobacterium tuberculosis Acquires Iron from Both Extracellular Transferrin and Intracellular Iron Pools
IMPACT OF INTERFERON-gamma AND HEMOCHROMATOSIS*

Oyebode OlakanmiDagger §, Larry S. SchlesingerDagger §||§§, Ambar AhmedDagger , and Bradley E. BritiganDagger §**Dagger Dagger

From the Dagger  Department of Internal Medicine and Research Service, Veteran Affairs Medical Center-Iowa City, Iowa City, Iowa 52246 and the Departments of § Internal Medicine and  Microbiology, the || Interdisciplinary Program in Immunology, and the ** Free Radical and Radiation Biology Program, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242

Mycobacterium tuberculosis multiplies within the macrophage phagosome and requires iron for growth. We examined the route(s) by which intracellular M. tuberculosis acquires iron. During intracellular growth of the virulent Erdman M. tuberculosis strain in human monocyte-derived macrophages (MDM), M. tuberculosis acquisition of 59Fe from transferrin (TF) provided extracellularly (exogenous source) was compared with acquisition when MDM were loaded with 59Fe from TF prior to M. tuberculosis infection (endogenous sources). M. tuberculosis 59Fe acquisition required viable bacteria and was similar from exogenous and endogenous sources at 24 h and greater from exogenous iron at 48 h. Interferon-gamma treatment of MDM reduced 59Fe uptake from TF 51% and TF receptor expression by 34%. Despite this, intraphagosomal M. tuberculosis iron acquisition in IFN-gamma -treated cells was decreased by only 30%. Macrophages from hereditary hemochromatosis patients have altered iron metabolism. Intracellular M. tuberculosis acquired markedly less iron in MDM from these individuals than in MDM from healthy donors, regardless of the iron source (exogenous and endogenous): 36 ± 3.8% and 17 ± 9.6% of control, respectively. Thus, intraphagosomal M. tuberculosis can acquire iron from both extracellular TF and endogenous macrophage sources. Acquisition of iron from macrophage cytoplasmic iron pools may be critical for the intracellular growth of M. tuberculosis. This acquisition is altered by IFN-gamma treatment to a small extent, but is markedly reduced in macrophages from hemochromatosis patients.

* This work was supported in part by Veteran Affairs Merit Review Grants (to B. E. B. and L. S. S.) and National Institutes of Health Grants AI24954 (to B. E. B.), AI33004 (to L. S. S.), and AI43870 (to L. S. S.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Dagger To whom correspondence should be addressed: University of Iowa Hospitals and Clinics, Dept. of Internal Medicine, Division of Infectious Diseases, SW54, GH, Iowa City, IA 52242. Fax: 319-356-4600; E-mail: bradley-britigan@uiowa.edu.

§§ Present address: Division of Infectious Diseases, Dept. of Medicine, Ohio State University, 4715 Cramblett Hall, 456 W. 10th Ave., Columbus, OH 43210. Fax: 614-293-5240; E-mail: schlesinger-2@medctr.osu.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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