Objective To reappraise the mouse model of ovalbumin (OVA)-induced asthma and to develop a new model of airway hyperresponsiveness (AHR) and its evaluation indicators.Methods Mice were sensitized with ovalbumin (OVA) and induced asthma by inhalation of 10% OVA at 15-21 days after the sensitization. The threshold value of capsaicin cough sensitivity test, and content of NO, ET-1, IL-13 in the lung homogenate were measured at 24 h after the last inhalation. Results The positive rate of cough reflex aroused by capsaicin was significantly increased with the raise of concentration of capsaicin (compared with the control group, P<0.01). The ED₅₀ of capsaicin cough of the model group was 89.39 μmol/L, significantly lower than that of the control group (204.84 μmol/L) and dexamethasone group (220.02 μmol/L). The contents of NO, ET-1, IL-13 in the lung homogenate of the model group were significantly increased, and dexamethasone significantly inhibited the increase of NO (compared with the control group, P<0.01).Conclusions The characteristics of the OVA-sensitized mouse model are resemble to that of clinical airway hyperresponsiveness. This model is simple to generate and stable, therefore, can be used as a model of AHR. The threshold value of capsaicin cough sensitivity test and the content of NO, ET-1, IL-13 in the lung homogenate can be used to evaluate the disease severity of the mouse models.