| First Author | Prakash H | Year | 2009 |
| Journal | PLoS One | Volume | 4 |
| Issue | 8 | Pages | e6519 |
| PubMed ID | 19657383 | Mgi Jnum | J:152480 |
| Mgi Id | MGI:4358828 | Doi | 10.1371/journal.pone.0006519 |
| Citation | Prakash H, et al. (2009) cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. PLoS One 4(8):e6519 |
| abstractText | The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. |
