Abstract:Objective To explore the role of IL-17 in the pathogenesis of asthmatic mice, and the relationship between the action mechanism of Budesonide controlling asthma and the expression level of IL-17. Methods Twenty-four female BALB/c mice at the age of 4 weeks were randomly divided into a control group, an asthma group and a Budesonide group, and each group had 8 mice. The mouse model of asthma was made by sensitization with ovalbumin (OVA). The asthmatic mice were treated with Budesonide suspension by atomization inhalation. After the success of the model, the pathological changes of the lung tissues were observed, and the expression level of IL-17 mRNA in the lung tissues was determined by qRT-PCR. The IL-17 level in the bronchoalveolar lavage fluid (BALF) was detected by ELISA. Results Compared with the control group, inflammatory cell infiltration in the airway of the asthma group and the expression level of IL-17 in BALF and IL-17 mRNA in the lung tissues were significantly higher (P < 0.05). After intervention with Budesonide atomization inhalation, the inflammatory cell infiltration in the airway and the expression level of IL-17 in BALF and IL-17 mRNA in the lung tissues in the Budesonide group were lower than those in the asthma group (P < 0.05). Conclusions The expression level of IL-17 is elevated in asthmtic mice. Inhibiting the expression level of IL-17 in mice is one of the mechanisms of Budesonide for asthma control.