| First Author | John AE | Year | 2005 |
| Journal | Eur J Immunol | Volume | 35 |
| Issue | 1 | Pages | 108-16 |
| PubMed ID | 15593301 | Mgi Jnum | J:95242 |
| Mgi Id | MGI:3525739 | Doi | 10.1002/eji.200425439 |
| Citation | John AE, et al. (2005) Respiratory syncytial virus-induced exaggeration of allergic airway disease is dependent upon CCR1-associated immune responses. Eur J Immunol 35(1):108-16 |
| abstractText | Severe respiratory syncytial virus (RSV) infection has a significant impact on airway function, and may alter subsequent development of asthma. CCR1 mRNA was significantly up-regulated during primary RSV infection in BALB/c mice, and was also up-regulated during allergen exposure in sensitized mice. Although CCR1(-/-) mice exhibited similar levels of airway hyperresponsiveness (AHR) as wild-type mice in response to cockroach allergen alone, in animals treated with RSV prior to cockroach antigen (CRA) sensitization and challenge, a significant decrease in exacerbated AHR was observed in the CCR1(-/-) mice. The reduction in AHR after RSV and allergen challenge in CCR1(-/-) mice was not associated with changes in peribronchial eosinophilia, but was accompanied by significantly decreased IL-13 levels in the lungs, as well as an absence of mucus cell staining within the airways. When T lymphocyte numbers were compared in animals receiving CRA to animals receiving a combination of RSV and allergen an increase in both CD4 and CD8 T lymphocytes could be detected in wild-type but not CCR1(-/-) animals. Thus, these data suggest that CCR1-mediated responses have a primary role for inducing severe disease during RSV infection, and may be responsible for altering the lung pathophysiological responses to subsequent allergen challenges via IL-13-mediated mechanisms. |
