This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brown, D. H.
Right arrow Articles by Zwilling, B. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brown, D. H.
Right arrow Articles by Zwilling, B. S.

 Previous Article  |  Next Article 

Infect. Immun., Feb 1997, 597-603, Vol 65, No. 2
Copyright © 1997, American Society for Microbiology

Stabilized expression of mRNA is associated with mycobacterial resistance controlled by Nramp1

DH Brown, WP Lafuse and BS Zwilling
Department of Microbiology, The Ohio State University, Columbus 43210, USA.

Control of innate resistance to the growth of mycobacteria is mediated by a gene termed Nramp1. Although the role of the protein product of Nramp1 in mediating resistance to mycobacterial growth is not known, the effect of the gene is pleiotropic and it has been suggested that the gene controls macrophage priming for activation. We have found that the functional capacity of macrophages from Mycobacterium bovis BCG- susceptible mice can be suppressed by corticosterone, while the function of macrophages from BCG-resistant mice remains unaffected. In this study, we show that corticosterone differentially affects the stability of mRNAs of several recombinant gamma interferon (rIFN-gamma)- induced genes. Treatment of macrophages from BCG-susceptible mice with corticosterone accelerates the decay of Nramp1 mRNA. The mRNA of IFN- gamma-induced genes of macrophages from BCG-resistant mice was more stable than the mRNA of macrophages from BCG-susceptible mice in the presence or absence of corticosterone. The results of this investigation suggest that Nramp1 acts by stabilizing the mRNA of genes associated with macrophage activation, thus accounting for the functional differences that have been attributed to these macrophage populations.


This article has been cited by other articles:

  • Gomez, M. A., Li, S., Tremblay, M. L., Olivier, M. (2007). NRAMP-1 Expression Modulates Protein-tyrosine Phosphatase Activity in Macrophages: IMPACT ON HOST CELL SIGNALING AND FUNCTIONS. J. Biol. Chem. 282: 36190-36198 [Abstract] [Full Text]  
  • Techau, M. E., Valdez-Taubas, J., Popoff, J.-F., Francis, R., Seaman, M., Blackwell, J. M. (2007). Evolution of Differences in Transport Function in Slc11a Family Members. J. Biol. Chem. 282: 35646-35656 [Abstract] [Full Text]  
  • White, J. K., Mastroeni, P., Popoff, J.-F., Evans, C. A. W., Blackwell, J. M. (2005). Slc11a1-mediated resistance to Salmonella enterica serovar Typhimurium and Leishmania donovani infections does not require functional inducible nitric oxide synthase or phagocyte oxidase activity. J. Leukoc. Biol. 77: 311-320 [Abstract] [Full Text]  
  • Fritsche, G., Dlaska, M., Barton, H., Theurl, I., Garimorth, K., Weiss, G. (2003). Nramp1 Functionality Increases Inducible Nitric Oxide Synthase Transcription Via Stimulation of IFN Regulatory Factor 1 Expression. J. Immunol. 171: 1994-1998 [Abstract] [Full Text]  
  • Wyllie, S., Seu, P., Gao, F. Q., Gros, P., Goss, J. A. (2002). Disruption of the Nramp1 (also known as Slc11a1) gene in Kupffer cells attenuates early-phase, warm ischemia-reperfusion injury in the mouse liver. J. Leukoc. Biol. 72: 885-897 [Abstract] [Full Text]  
  • Wardrop, S. L., Wells, C., Ravasi, T., Hume, D. A., Richardson, D. R. (2002). Induction of Nramp2 in activated mouse macrophages is dissociated from regulation of the Nramp1, classical inflammatory genes, and genes involved in iron metabolism. J. Leukoc. Biol. 71: 99-106 [Abstract] [Full Text]  
  • Zhong, W., Lafuse, W. P., Zwilling, B. S. (2001). Infection with Mycobacterium avium Differentially Regulates the Expression of Iron Transport Protein mRNA in Murine Peritoneal Macrophages. Infect. Immun. 69: 6618-6624 [Abstract] [Full Text]  
  • Zhang, G., Wu, H., Ross, C. R., Minton, J. E., Blecha, F. (2000). Cloning of Porcine NRAMP1 and Its Induction by Lipopolysaccharide, Tumor Necrosis Factor Alpha, and Interleukin-1beta : Role of CD14 and Mitogen-Activated Protein Kinases. Infect. Immun. 68: 1086-1093 [Abstract] [Full Text]  
  • Wright, A. D., Chapes, S. K. (1999). LPS sensitivity in recombinant mice lacking functional alleles at MHCII, Lps and Nramp1 genes. Innate Immunity 5: 297-305 [Abstract]  
  • Searle, S., Blackwell, J. M (1999). Evidence for a functional repeat polymorphism in the promoter of the human NRAMP1 gene that correlates with autoimmune versus infectious disease susceptibility. J. Med. Genet. 36: 295-299 [Abstract] [Full Text]  
  • Zwilling, B. S., Kuhn, D. E., Wikoff, L., Brown, D., Lafuse, W. (1999). Role of Iron in Nramp1-Mediated Inhibition of Mycobacterial Growth. Infect. Immun. 67: 1386-1392 [Abstract] [Full Text]  
  • Searle, S, Bright, N., Roach, T., Atkinson, P., Barton, C., Meloen, R., Blackwell, J. (1998). Localisation of Nramp1 in macrophages: modulation with activation and infection. J. Cell Sci. 111: 2855-2866 [Abstract]