| First Author | Matsuyama M | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 1 | Pages | e0147064 |
| PubMed ID | 26784959 | Mgi Jnum | J:248889 |
| Mgi Id | MGI:6092581 | Doi | 10.1371/journal.pone.0147064 |
| Citation | Matsuyama M, et al. (2016) Overexpression of RORgammat Enhances Pulmonary Inflammation after Infection with Mycobacterium Avium. PLoS One 11(1):e0147064 |
| abstractText | Mycobacterium avium complex (MAC) is the most common cause of nontuberculous mycobacterial disease in humans. The role of Th17 immunity in the pathogenesis of intracellular bacteria, such as MAC, is not currently understood. Transcription factor RAR-related orphan receptor gamma t (RORgammat) is known as the master regulator for Th17 cell development. Here, we investigated the role of RORgammat in host responses against MAC infection. Wild-type (WT) mice and RORgammat-overexpressing mice were infected with MAC via intratracheal inoculation. Systemic MAC growth was not different between WT mice and RORgammat-overexpressing mice. However, neutrophilic pulmonary inflammation following MAC infection was enhanced in RORgammat-overexpressing mice compared with that in WT mice. The cytokine expression shifted toward a Th17 phenotype in the lungs of RORgammat-overexpressing mice following MAC infection; the levels of IL-6 and IL-17 were significantly higher in the lung of these mice than in WT mice. In addition to the increase in IL-17 single-positive T cells, T cells producing both IL-17 and interferon-gamma were elevated in the lung of RORgammat-overexpressing mice following MAC infection. These findings suggest that RORgammat overexpression-mediated Th17 bias contributes to local inflammation rather than systemic responses, by regulating neutrophil recruitment into the sites of infection during MAC infection. |
