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Respiratory syncytial virus-induced exaggeration of allergic airway disease is dependent upon CCR1-associated immune responses.

Authors: John, AE  Gerard, CJ  Schaller, M  Miller, AL  Berlin, AA  Humbles, AA  Lukacs, NW 
Citation: John AE, etal., Eur J Immunol. 2005 Jan;35(1):108-16.
Pubmed: (View Article at PubMed) PMID:15593301
DOI: Full-text: DOI:10.1002/eji.200425439

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.


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CRRD Object Information
CRRD ID: 5688159
Created: 2012-02-20
Species: All species
Last Modified: 2012-02-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.