Abstract (EN):
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-gamma and TNF-alpha 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-gamma 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.
Language:
English
Type (Professor's evaluation):
Scientific
No. of pages:
6