Deletion of CCR1 attenuates pathophysiologic responses during respiratory syncytial virus infection.

The role of chemokines in chronic inflammatory responses are central to the recruitment of particular subsets of leukocytes. In the present studies, we have examined the role of CCR1 in the developing pathogenesis of respiratory syncytial virus (RSV) in the lungs of infected BALB/c mice. Although we did not observe significant differences in clearance of RSV, we were able to identify decreased pathophysiologic responses in CCR1(-/-) mice.

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

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.