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Infect. Immun., Feb 1997, 597-603, Vol 65, No. 2
DH Brown, WP Lafuse and BS Zwilling
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.
Copyright © 1997, American Society for Microbiology
Stabilized expression of mRNA is associated with mycobacterial resistance controlled by Nramp1
Department of Microbiology, The Ohio State University, Columbus 43210, USA.
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