One mechanism of glucocorticoid action in asthma may involve the inhibition of IL-25 expression

  • Authors:
    • Wei Lu
    • Chao Lu
    • Chengming Zhang
    • Chenghao Zhang
  • View Affiliations

  • Published online on: December 27, 2016     https://doi.org/10.3892/etm.2016.4002
  • Pages: 657-661
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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.

Related Articles

Journal Cover

February-2017
Volume 13 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Lu W, Lu C, Zhang C and Zhang C: One mechanism of glucocorticoid action in asthma may involve the inhibition of IL-25 expression. Exp Ther Med 13: 657-661, 2017
APA
Lu, W., Lu, C., Zhang, C., & Zhang, C. (2017). One mechanism of glucocorticoid action in asthma may involve the inhibition of IL-25 expression. Experimental and Therapeutic Medicine, 13, 657-661. https://doi.org/10.3892/etm.2016.4002
MLA
Lu, W., Lu, C., Zhang, C., Zhang, C."One mechanism of glucocorticoid action in asthma may involve the inhibition of IL-25 expression". Experimental and Therapeutic Medicine 13.2 (2017): 657-661.
Chicago
Lu, W., Lu, C., Zhang, C., Zhang, C."One mechanism of glucocorticoid action in asthma may involve the inhibition of IL-25 expression". Experimental and Therapeutic Medicine 13, no. 2 (2017): 657-661. https://doi.org/10.3892/etm.2016.4002