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Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal
Mice genetically deficient in the inducible NO synthase gene
(iNOS-/-) were used to study the role played by NO during infection
by Mycobacterium avium. iNOS-/- macrophages were
equally able to restrict M. avium growth in vitro
following stimulation by IFN-
and TNF-
as macrophages from
wild-type mice. In vivo, the infection progressed at similar rates in
wild-type and NO-deficient mice during the first 2 mo of infection, but
the latter mice were subsequently more efficient in clearing the
mycobacteria than the former. The increased resistance of iNOS-/-
mice was associated with higher IFN- levels in the serum and
following in vitro restimulation of spleen cells with specific Ag,
increased formation of granulomas and increased survival of
CD4+ T cells. We show that NO is not involved in the
antimycobacterial mechanisms of M. avium-infected
macrophages and, furthermore, that it exacerbates the infection by
causing the suppression of the immune response to the
pathogen.
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