| First Author | Kuchtey J | Year | 2006 |
| Journal | Immunology | Volume | 118 |
| Issue | 1 | Pages | 39-49 |
| PubMed ID | 16630021 | Mgi Jnum | J:109682 |
| Mgi Id | MGI:3629462 | Doi | 10.1111/j.1365-2567.2006.02337.x |
| Citation | Kuchtey J, et al. (2006) Interferon-alphabeta mediates partial control of early pulmonary Mycobacterium bovis bacillus Calmette-Guerin infection. Immunology 118(1):39-49 |
| abstractText | The role of type I interferon (IFN-alphabeta) in modulating innate or adaptive immune responses against mycobacterial infection in the lung is unclear. In this study we investigated the susceptibility of IFN-alphabeta-receptor-deficient (IFN-alphabetaR-/-) mice to pulmonary infection with aerosolized Mycobacterium bovis bacillus Calmette-Guerin (BCG). During early infection (2-3 weeks), enhanced growth of BCG was measured in the lungs of IFN-alphabetaR-/- mice compared to wild-type mice. However, during late infection the burden of BCG was similar in the lungs of IFN-alphabetaR-/- and wild-type mice. Although control of BCG growth was delayed, recruitment and activation of T and natural killer cells, production of IFN-gamma, and cytokine expression were all similar in wild-type and IFN-alphabetaR-/- mice. However, decreased expression of nitric oxide in bronchoalveolar lavage fluids from IFN-alphabetaR-/- mice correlated with enhanced growth of BCG. Bone marrow-derived macrophages from IFN-alphabetaR-/- mice also produced less nitric oxide following infection with BCG in vitro. These findings suggest that IFN-alphabeta contributes to innate immunity to pulmonary mycobacterial infection by augmenting production of nitric oxide. |
