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Blood, 1 August 2008, Vol. 112, No. 3, pp. 866-874. Prepublished online as a Blood First Edition Paper on March 27, 2008; DOI 10.1182/blood-2007-12-126854. This Article Full Text (PDF) All Versions of this Article: blood-2007-12-126854v1 112/3/866    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Paradkar, P. Articles by Ward, D. M. Search for Related Content PubMed PubMed Citation Articles by Paradkar, P. Articles by Ward, D. M. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 7, 2007 Accepted March 18, 2008 Iron-depletion limits intracellular bacterial growth in macrophages Prasad Paradkar, Ivana De Domenico, Nina Durchfort, Irene Zohn, Jerry Kaplan, and Diane McVey Ward* Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT, United States Center for Neuroscience Research, Children's National Medical Center, Washington, D.C., United States * Corresponding author; email: diane.mcveyward{at}path.utah.edu. Many intracellular pathogens infect macrophages and these pathogens require iron for growth. Here we demonstrate in vitro that the intracellular growth of Chlamydia psittaci, Chlamydia trachomatis and Legionella pneumophila is regulated by the levels of intracellular iron. Macrophages that express cell surface ferroportin, the only known cellular iron exporter, limit the intracellular growth of these bacteria. Hepcidin is an anti-microbial peptide secreted by the liver in response to inflammation. Hepcidin binds to ferroportin mediating its internalization and degradation. Addition of hepcidin to infected macrophages enhanced the intracellular growth of these pathogens. Macrophages from flatiron mice, a strain heterozygous for a loss-of-function ferroportin mutation, showed enhanced intracellular bacterial growth independent of the presence of exogenous hepcidin. Macrophages, from wild type or flatiron mice, incubated with the oral iron chelators deferriprone or desferasirox showed reduced intracellular bacterial growth suggesting that these chelators might be therapeutic in chronic intracellular bacterial infections CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: The irony of host defense Marianne Wessling-Resnick Blood 2008 112: 460. [Full Text] [PDF] This article has been cited by other articles: M. Nairz, I. Theurl, A. Schroll, M. Theurl, G. Fritsche, E. Lindner, M. Seifert, M.-L. V. Crouch, K. Hantke, S. Akira, et al. Absence of functional Hfe protects mice from invasive Salmonella enterica Serovar Typhimurium infection via induction of lipocalin-2 Blood, October 22, 2009; 114(17): 3642 - 3651. [Abstract] [Full Text] [PDF] M. van Deuren, J. J. C. Kroot, and D. W. Swinkels Time-course analysis of serum hepcidin, iron and cytokines in a C282Y homozygous patient with Schnitzler's syndrome treated with IL-1 receptor antagonist Haematologica, September 1, 2009; 94(9): 1297 - 1300. [Abstract] [Full Text] [PDF] C. L. Koening, J. C. Miller, J. M. Nelson, D. M. Ward, J. P. Kushner, L. K. Bockenstedt, J. J. Weis, J. Kaplan, and I. De Domenico Toll-like receptors mediate induction of hepcidin in mice infected with Borrelia burgdorferi Blood, August 27, 2009; 114(9): 1913 - 1918. [Abstract] [Full Text] [PDF] D. Prantner and U. M. Nagarajan Role for the Chlamydial Type III Secretion Apparatus in Host Cytokine Expression Infect. Immun., January 1, 2009; 77(1): 76 - 84. [Abstract] [Full Text] [PDF] J. F. Collins, M. Wessling-Resnick, and M. D. Knutson Hepcidin Regulation of Iron Transport J. Nutr., November 1, 2008; 138(11): 2284 - 2288. [Abstract] [Full Text] [PDF]

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