While the mechanism of action of classic cytokines in asthma has received increased attention from researchers, certain non‑classical cytokines, such as IL‑25, also participate in this mechanism. The present study was performed to investigate the changes in IL‑25 (IL‑17E) mRNA and protein in bronchial asthma and to further characterize the mechanism underlying the action of glucocorticoids in asthma. A total of 96  specific pathogen‑free BALB/c male mice were randomly divided into three normal groups (after the first allergization, after the second allergization and after excitation), three asthma groups (with the same three subgroups), a dexamethasone group and a budesonide group (n=12/group). An asthma model was established via the ovalbumin‑sensitized excitation method. Mice in the dexamethasone group received intraperitoneal injections of dexamethasone 1 h prior to each excitation, the budesonide group received a budesonide suspension via inhalation 2 h before and after each provocation, and the normal group was sensitized and challenged with isotonic saline. IL‑25 protein expression levels in the bronchoalveolar lavage fluid were measured by ELISA, and the relative IL‑25 mRNA content in lung tissue was determined by reverse transcription‑quantitative polymerase chain reaction. Compared with the normal groups, both the protein and mRNA levels of IL‑25 were significantly increased (P<0.05) in the asthma groups. Dexamethasone and budesonide groups exhibited significant protein and mRNA reductions in IL‑25, as compared with the asthma group after excitation (P<0.05), whereas these two groups significantly increased levels compared with the normal group after excitation (P<0.05). No significant differences in IL‑25 mRNA expression levels were detected in the dexamethasone and budesonide groups when compared with the normal group after excitation. Therefore, we conclude that IL‑25 is involved throughout the process of inflammation and inflammatory immune pathogenesis in asthma. One of the mechanisms of glucocorticoid action in asthma may involve inhibition of IL-25 expression.

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