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Infection and Immunity, November 2001, p. 6618-6624, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6618-6624.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Infection with Mycobacterium avium Differentially Regulates the Expression of Iron Transport Protein mRNA in Murine Peritoneal Macrophages

Wangjian Zhong,1 William P. Lafuse,2 and Bruce S. Zwilling1,2,*

Department of Microbiology, College of Biological Sciences,1 and Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health,2 The Ohio State University, Columbus, Ohio 43210

Received 17 May 2001/Returned for modification 7 July 2001/Accepted 6 August 2001

Iron is an important element for the growth of microorganisms as well as in the defense of the host by serving as a catalyst for the generation of free radicals via the Fenton/Haber-Weiss reactions. The iron transporter natural resistance-associated macrophage protein 1 (Nramp1) confers resistance to the growth of a variety of intracellular pathogens including Mycobacterium avium. Recently several other proteins that are involved in iron transport, including the highly homologous iron transporter Nramp2 and the transferrin receptor-associated protein HFE (hereditary hemochromatosis protein), have been described. The relationship of these proteins to host defense and to the growth of intracellular pathogens is not known. Here, we report that infection with M. avium differentially regulates mRNA expression of the proteins associated with iron transport in murine peritoneal macrophages. Both Nramp1 and Nramp2 mRNA levels increase following infection, while the expression of transferrin receptor mRNA decreases. The level of expression of HFE mRNA remains unchanged. The difference in the expression of the mRNA of these proteins following infection or cytokine stimulation suggests that they may play an important role in host defense by maintaining a delicate balance between iron availability for host defense and at the same time limiting iron availability for microbial growth.

* Corresponding author. Mailing address: Department of Microbiology, The Ohio State University, 484 West 12th Ave., Columbus, OH 43210. Phone: (614) 292-3310. Fax: (614) 292-8120. E-mail: zwilling.1{at}osu.edu.

Infection and Immunity, November 2001, p. 6618-6624, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6618-6624.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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