Lu Wei, Lu Chao, Zhang Chengming, Zhang Chenghao
Department of Pediatrics, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Department of Gynecology and Obstetrics, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Exp Ther Med. 2017 Feb;13(2):657-661. doi: 10.3892/etm.2016.4002. Epub 2016 Dec 27.
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.
虽然经典细胞因子在哮喘中的作用机制已受到研究人员越来越多的关注，但某些非经典细胞因子，如白细胞介素-25（IL-25），也参与这一机制。本研究旨在调查支气管哮喘中IL-25（IL-17E）mRNA和蛋白的变化，并进一步阐明糖皮质激素在哮喘中作用的潜在机制。总共96只无特定病原体的BALB/c雄性小鼠被随机分为三个正常组（首次致敏后、第二次致敏后和激发后）、三个哮喘组（具有相同的三个亚组）、一个地塞米松组和一个布地奈德组（每组n = 12）。通过卵清蛋白致敏激发法建立哮喘模型。地塞米松组小鼠在每次激发前1小时腹腔注射地塞米松，布地奈德组在每次激发前后2小时通过吸入给予布地奈德混悬液，正常组用等渗盐水致敏和激发。采用酶联免疫吸附测定法检测支气管肺泡灌洗液中IL-25蛋白表达水平，通过逆转录-定量聚合酶链反应测定肺组织中相对IL-25 mRNA含量。与正常组相比，哮喘组中IL-25的蛋白和mRNA水平均显著升高（P<0.05）。与激发后的哮喘组相比，地塞米松组和布地奈德组的IL-25蛋白和mRNA水平显著降低（P<0.05），而与激发后的正常组相比，这两组水平显著升高（P<0.05）。与激发后的正常组相比，地塞米松组和布地奈德组的IL-25 mRNA表达水平未检测到显著差异。因此，我们得出结论，IL-25参与哮喘炎症和炎症免疫发病机制的全过程。糖皮质激素在哮喘中发挥作用的机制之一可能涉及抑制IL-25表达。
