Improved Clearance of Mycobacterium avium Upon Disruption of the Inducible Nitric Oxide Synthase Gene

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 wil...

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Published inThe Journal of immunology (1950) Vol. 162; no. 11; pp. 6734 - 6739
Main Authors Gomes, M. Salome, Florido, Manuela, Pais, Teresa F, Appelberg, Rui
Format Journal Article
LanguageEnglish
Published United States Am Assoc Immnol 01.06.1999
Subjects
Animals
Female
Interferon-gamma - biosynthesis
Interferon-gamma - physiology
Macrophages - enzymology
Macrophages - immunology
Macrophages - microbiology
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Mice, Knockout
Mycobacterium avium
Mycobacterium avium - growth & development
Mycobacterium avium - immunology
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Species Specificity
Tuberculosis - enzymology
Tuberculosis - immunology
Tuberculosis - microbiology
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Abstract 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.
AbstractList 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.
Abstract 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-γ and TNF-α 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-γ 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.
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 super(+) T cells. We show that NO is not involved in the antimycobacterial mechanisms of M. avium-infected macrophages and, further-more, that it exacerbates the infection by causing the suppression of the immune response to the pathogen.
Author Gomes, M. Salome
Appelberg, Rui
Florido, Manuela
Pais, Teresa F
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Snippet Mice genetically deficient in the inducible NO synthase gene (iNOS-/-) were used to study the role played by NO during infection by Mycobacterium avium....
Abstract Mice genetically deficient in the inducible NO synthase gene (iNOS−/−) were used to study the role played by NO during infection by Mycobacterium...
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SubjectTerms Animals
Female
Interferon-gamma - biosynthesis
Interferon-gamma - physiology
Macrophages - enzymology
Macrophages - immunology
Macrophages - microbiology
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Mice, Knockout
Mycobacterium avium
Mycobacterium avium - growth & development
Mycobacterium avium - immunology
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Species Specificity
Tuberculosis - enzymology
Tuberculosis - immunology
Tuberculosis - microbiology
Title Improved Clearance of Mycobacterium avium Upon Disruption of the Inducible Nitric Oxide Synthase Gene
URI http://www.jimmunol.org/cgi/content/abstract/162/11/6734
https://www.ncbi.nlm.nih.gov/pubmed/10352292
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