Objective:To investigate the inhibitory effects of budesonide on the expression of OX40(CD134),airway inflammation,and airway hyperresponsiveness in a murine model of asthma. Methods:Total 18 BALB/c mice were randomly divided into 3 groups. They were control group,ovalbumin (OVA) group and budesonide group. Mice were sensitized and challenged by OVA. Airway responsiveness to acetylcholine chloride was measured. Hematoxylin & eosin staining was used to assess the inflammatory cell infiltrates. Levels of IL-4 and IL-13 in bronchoalveolar lavage fluid(BALF),and total IgE and OVA-specific IgE(OVA-sIgE) in serum were detected by ELISA. The protein expression of OX40 was determined by Western blot analysis. Results:The airway resistance in the OVA group was obviously increased in a dose-dependent manner by administration of ACh,whereas only a slight increase could be detected in the control group. There were no significant differences in baseline airway resistance among three groups(P > 0.05). Treatment with budesonide led to a sharp decrease in airway resistance compared with the OVA group (P < 0.05). The number of eosinophils and total inflammatory cells in BALF in the OVA group increased significantly compared with the control group (P < 0.05),which was significantly decreased by treatment with budesonide(P < 0.05). The levels of the IL-4 and IL-13 in BALF,and the levels of total serum IgE and OVA-sIgE were significantly increased in OVA-sensitized/challenged mice compared with the control group (P < 0.05). Administration of budesonide reduced the levels of those Th2 cytokines in BALF,and the levels of total serum IgE and OVA-sIgE,when compared with the OVA group(P < 0.05). Treatment with budesonide increased the ratio of OX40,compared with that in the OVA group (P < 0.05). Conclusion:Budesonide could inhibit the airway inflammation and hyperresponsivenes by down-regulating the expression of OX40.