Objective: To investigate the inflammatory changes and the airway hyper-responsiveness in the asthma mouse model infected by respiratory syncytial virus and elucidate the relationship between the infection and the effect of glucocorticoid.;-;Methods: 60 BALB/c mice were randomly divided into 6 groups. One of these is the control group; the others are the OVA/sham group, the OVA/sham +Dex group, the PBS/RSV group, the OVA/RSV group and the OVA/RSV+Dex group. The airway resistance was measured using a sealed body plethysmograph. Pathological slides were stained with hematoxylin-eosin, and the peribronchial inflammation was observed microscopically. The concentrations of IL-4, IFN-gamma, TGF-beta(1) in lung tissues were detected by ELISA.;-;Results: Compared with the control group, the degree of the airway inflammation and hyperresponsiveness and the concentrations of IL-4/IFN-gamma,. TGF-beta(1) in all four OVA groups increased significantly. And there was a statistically significant difference between the OVA/sham group and the OVA/sham+Dex group, and between the OVA/RSV group and the OVA/RSV+Dex group respectively. Compared with the OVA/RSV group, there was an obvious aggravation of airway inflammation and hyperresponsiveness in the OVA/RSV+Dex group.;-;Conclusions: Glucocorticoid significantly reduces airway inflammation and hyper-responsiveness induced by repetitive OVA challenge in the mouse model of asthma. However, the significant decrease in Th-1 and increase in Th-2 inflammation and aggravation of airway hyper-responsiveness in the mice in OVA/RSV group show that they are not sensitive to glucocorticoid. The effects of infection with RSV on the mouse model of asthma could be the cause of the glucocorticoid resistance during the therapy. (Asian Pac J Allergy Immunol 2011;29:176-80)