Respiratory syncytial virus‐induced CCL5/RANTES contributes to exacerbation of allergic airway inflammation

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Abstract
Severe respiratory syncytial virus (RSV) infection has a significant impact on airway function and may induce or exacerbate the response to a subsequent allergic challenge. In a murine model combining early RSV infection with later cockroach allergen (CRA) challenge, we examined the role of RSV‐induced CCL5/RANTES production on allergic airway responses. RSV infection increased CCL5 mRNAand protein levels, peaking at days 8 and 12, respectively. Administration of CCL5 antiserum during days 0–14 of the RSV infection did not significantly alter viral protein expression when comparedto mice treated with control serum. In mice receiving the combined RSV‐allergen challenge, lungs collected on day 22 exhibited significantly increased numbers of CD4‐ and CD8‐positive T cells. Thisincrease in T cell numbers was not observed in mice receiving α‐CCL5. On day 43, peribronchial eosinophilia and leukotriene levels were increased in RSV‐allergen mice. Pretreatment with CCL5 antiserum resulted in decreased recruitment of inflammatory cells to bronchoalveolar and peribronchial regions of the lungs and these reductions were associated with a reduction in both T cell recruitment into the bronchoalveolar space, leukotriene release and chemokine generation. Thus, CCL5 released during RSV infection has a significant effect on the inflammatory response to subsequent allergic airway challenges.