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*
Department of Microbiology, College of Biological Sciences, and
Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health, Ohio State University, Columbus, OH 43210
Recent studies have implicated Toll-like receptors (TLR),
especially TLR2 and TLR4, as sentinel receptors that signal the
interaction of macrophages with bacterial pathogens via a
NF-
B-mediated pathway. The regulation of TLR gene expression,
however, has not been intensively studied. Here, we report that TLR2
mRNA was induced following infection of murine macrophages with
Mycobacterium avium. The changes in TLR2 mRNA correlated
with an increase in TLR2 surface expression. Infection with M.
avium resulted in a concomitant decrease in TLR4 mRNA. The
effect of M. avium infection on TLR2 mRNA appeared to be
mediated, in part, by TLR2 because the induction of the mRNA was
partially blocked by preincubation of the macrophages with an
anti-human TLR2 Ab. In contrast, the effect of LPS stimulation was
mediated via TLR4 because infection of macrophages from
LPSd mice, which do not express active TLR4, resulted in an
increase in TLR2 mRNA, while treatment of macrophages from these mice
with LPS failed to induce TLR2 mRNA. Several cytokines, including
TNF-
, IL-1, and GM-CSF, but not IFN-
, induced TLR2 mRNA.
M. avium infection resulted in the induction of TLR2
mRNA by macrophages from both TNFRI knockout and NF-B p50 knockout
mice.
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