Respiratory syncytial virus enhances the expression of CD11b molecules and the generation of superoxide anion by human eosinophils primed with platelet-activating factor.

BACKGROUND

Human respiratory syncytial virus (RSV) infection in infancy and early childhood causes acute bronchiolitis and exacerbates bronchial asthma. Eosinophil infiltration may contribute to airway obstruction in RSV infection.

OBJECTIVE

We hypothesized that RSV affects eosinophil function.

METHODS

Eosinophil activation was evaluated by chemiluminescent detection of superoxide anion (O(2)(-)) generation. Expression of CD11b on eosinophils was determined by flow cytometry.

RESULTS

Although RSV did not induce O(2)(-) generation by resting eosinophils, RSV enhanced O(2)(-) generation of eosinophils primed with platelet-activating factor (PAF). Enhancement was significantly inhibited by either continuous agitation to prevent eosinophil adhesion to test tube surfaces or by pretreating cells with anti-CD18 antibody, suggesting that the stimulatory effects of RSV on eosinophils depend on cell adhesion via beta(2)-integrins. In fact, RSV enhanced PAF-induced CD11b expression by eosinophils. CONCLUSIONS These findings suggest that RSV enhances eosinophil CD11b expression and O(2)(-) generation induced by PAF. Thus, RSV infection may exacerbate airway inflammation by enhancing mediator release from eosinophils.