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

D H Brown1, W P Lafuse, B S Zwilling

  • 1Department of Microbiology, The Ohio State University, Columbus 43210, USA.

Infection and Immunity
|February 1, 1997
PubMed

Insights

The Nramp1 gene controls innate resistance to mycobacteria by stabilizing messenger RNA (mRNA) crucial for macrophage activation. Corticosterone affects Nramp1 mRNA stability differently in resistant versus susceptible mice.

Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Innate resistance to mycobacteria is regulated by the Nramp1 gene.
  • The precise function of the Nramp1 protein in mycobacterial resistance is unclear, but it's thought to prime macrophages for activation.
  • Corticosterone suppresses macrophage function in Mycobacterium bovis BCG-susceptible mice but not in BCG-resistant mice.

Purpose of the Study:

  • To investigate how corticosterone differentially affects the stability of messenger RNAs (mRNAs) induced by recombinant gamma interferon (rIFN-gamma).
  • To elucidate the role of Nramp1 in macrophage activation and its interaction with corticosterone.

Main Methods:

  • Treatment of macrophages from BCG-susceptible and BCG-resistant mice with corticosterone.
  • Analysis of the stability of Nramp1 mRNA and other rIFN-gamma-induced gene mRNAs.
  • Comparison of mRNA decay rates in the presence and absence of corticosterone.

Main Results:

  • Corticosterone accelerates Nramp1 mRNA decay in macrophages from BCG-susceptible mice.
  • Macrophages from BCG-resistant mice exhibit more stable mRNA for rIFN-gamma-induced genes compared to susceptible mice, irrespective of corticosterone treatment.
  • Differential mRNA stability correlates with functional differences in macrophage populations.

Conclusions:

  • Nramp1 likely functions by enhancing the stability of mRNAs involved in macrophage activation.
  • The findings suggest a mechanism for Nramp1-mediated control of innate resistance to mycobacteria, influenced by corticosterone.

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