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目的白介素5(IL-5)作为参与嗜酸粒细胞(EOS)成熟、分化过程的最主要因子,其作用通过特异性受体白介素5受体α链(IL-5Rα)介导。本研究以支气管上皮细胞株为研究对象,发现支气管上皮细胞在炎症因子的刺激下可以表达IL-5Rα。方法通过促炎症因子肿瘤坏死因子α(TNF-α)和Th2型细胞因子IL-4,IL-5,IL-13以及白三烯成分之一的白三烯C4(LTC4)对细胞进行单独或协同刺激,以逆转录聚合酶链反应(RT-PCR)方法、流式细胞检测技术评价上皮细胞对IL-5Rα的基因和蛋白质的表达,同时评价在IL-5和TNF-α的协同刺激下IL-5Rα、细胞内黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)的协同表达。结果正常支气管上皮细胞在Th2型细胞因子、LTC4和TNF-α的刺激下可以表达IL-5Rα基因,在TNF-α单独或与其他因子的协同刺激下表达显著增强,更可以表达IL-5Rα蛋白。流式细胞检测分析显示TNF-α单独或协同刺激后16hIL-5Rα蛋白表达最高,并随时间的延长表达下降。当TNF-α与IL-5协同刺激后上皮细胞可以同时表达VCAM-1和IL-5Rα,而ICAM-1呈持续表达。结论本研究通过对支气管上皮细胞的研究证实了支气管上皮细胞可以在炎症因子TNF-α和Th2型细胞因子的协同刺激下进一步表达IL-5特异性受体IL-5Rα,并在IL-5和TNF-α的刺激下进一步表达黏附分子VCAM-1,吸引EOS及其前体细胞浸润至气道参与炎症。说明支气管上皮细胞不仅在支气管哮喘炎症反应中是最主要的受累器官,也是导致炎症的参与者之一。
Objective Interleukin-5 (IL-5) is the most important factor involved in the maturation and differentiation of eosinophils (EOS), and its role is mediated by the specific receptor interleukin 5 receptor α chain (IL-5Rα). In this study, the bronchial epithelial cell line was selected as the research object and found that bronchial epithelial cells can express IL-5Rα under the stimulation of inflammatory cytokines. Methods Cells were treated with pro-inflammatory cytokines TNF-α and Th2 cytokines IL-4, IL-5, IL-13 and leukotriene C4 (LTC4) Synergistic stimulation was used to evaluate the expression of IL-5Rα gene and protein in epithelial cells by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry (FCM). Meanwhile, IL-5 and TNF-α The synergistic expression of IL-5Rα, ICAM-1 and VCAM-1. Results The normal bronchial epithelial cells could express IL-5Rα gene stimulated by Th2 cytokines, LTC4 and TNF-α, which were significantly enhanced under the stimulation of TNF-α alone or in combination with other factors, and could express IL-5Rα protein . Flow cytometry analysis showed that IL-5Rα protein expression was highest at 16 h after TNF-α stimulation alone or synergistically, and decreased with time. The epithelial cells could express VCAM-1 and IL-5Rα simultaneously when TNF-α and IL-5 were stimulated, while ICAM-1 was continuously expressed. Conclusion Our study on bronchial epithelial cells confirmed that bronchial epithelial cells can further express IL-5Rα, an IL-5 receptor specific receptor, in the presence of IL-5 and TNF-α stimulated further expression of adhesion molecule VCAM-1, to attract EOS and its precursor cells infiltrated into the airway to participate in inflammation. Bronchial epithelial cells not only in bronchial inflammatory response is the most important organ involved, but also lead to inflammation of the participants.