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Interferon‐αβ mediates partial control of early pulmonary Mycobacterium bovis bacillus Calmette–Guérin infection
Author(s) -
Kuchtey John,
Fulton Scott A.,
Reba Scott M.,
Harding Clifford V.,
Boom W. Henry
Publication year - 2006
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2006.02337.x
Subject(s) - mycobacterium bovis , bronchoalveolar lavage , immunology , biology , interferon gamma , nitric oxide , innate immune system , cytokine , interferon , lung , microbiology and biotechnology , immunity , immune system , mycobacterium tuberculosis , tuberculosis , medicine , pathology , endocrinology
Summary The role of type I interferon (IFN‐αβ) in modulating innate or adaptive immune responses against mycobacterial infection in the lung is unclear. In this study we investigated the susceptibility of IFN‐αβ‐receptor‐deficient (IFN‐αβR –/– ) mice to pulmonary infection with aerosolized Mycobacterium bovis bacillus Calmette–Guérin (BCG). During early infection (2–3 weeks), enhanced growth of BCG was measured in the lungs of IFN‐αβR –/– mice compared to wild‐type mice. However, during late infection the burden of BCG was similar in the lungs of IFN‐αβR –/– and wild‐type mice. Although control of BCG growth was delayed, recruitment and activation of T and natural killer cells, production of IFN‐γ, and cytokine expression were all similar in wild‐type and IFN‐αβR –/– mice. However, decreased expression of nitric oxide in bronchoalveolar lavage fluids from IFN‐αβR –/– mice correlated with enhanced growth of BCG. Bone marrow‐derived macrophages from IFN‐αβR –/– mice also produced less nitric oxide following infection with BCG in vitro . These findings suggest that IFN‐αβ contributes to innate immunity to pulmonary mycobacterial infection by augmenting production of nitric oxide.