白细胞介素5受体α链在支气管上皮细胞BEAS-2B的表达

The IL-5 receptor expression on bronchial epithelial cell line-BEAS-2B

目的白细胞介素5（n5）作为参与嗜酸粒细胞成熟、分化过程的最主要因子，其作用通过特异性受体IL-5Rα介导。本文以支气管上皮细胞株为研究对象，证实该上皮细胞株在炎症因子的刺激下可以表达IL-5Rα。方法通过促炎症因子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LTC4（白三烯C4）对细胞进行单独或协同刺激，以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、ICAM-1和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16h IL-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仆Bα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，吸引嗜酸粒细胞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 To investigate IL-5Rα gene and protein expression on bronchial epithelial cell line-BEAS-2B cell under the stimulation of inflammatory agents. Methods Human bronchial epithelial cell line BEAS-2B cells were investigated after stimulation by TNF-α, IL-5, IL-4, IL-13 and LTC4. RT-PCR was used to evaluate IL-5Rα gene expression and flow cytometry was used to assess IL-5Rα protein expression. We also investigate BEAS-2B cell on ICAM-1, VCAM-1 and IL-5Rα coordinate expression under the stimulation of TNF-α and IL-5. Results TH2 cytokines and leukotriene CA can stimulate BEAS-2B cell to express IL-5Rα gene to some extent. Those groups stimulated by TNF-α alone or TNF-α combine with other cytokines strongly expressed IL-5Rα gene. Detected by flow cytometry, BEAS-2B cell stimulated by TNF-α alone or combine with other cytokines for 16 hours can express IL-5Rα protein as compare to the unstimulated cells or stimulated with TH2 cytokines and LTC4 alone. Along with the stimulation time, IL-5Rα protein expression decreased. Both VCAM-1 and IL-5Rα protein expression elevated by the stimulation of TNF-α combination with IL-5, while ICAM-1 was consecutively expressed on bronchial epithelial cell. Conclusion IL-5Rα gene was expressed on BEAS-2B cell under the stimulation of inllammatory agents. IL-5 and TNF-α can increase bronchial epithelial cell to express IL-5Rα and adhesion molecule- VCAM-1, then to attract eosinophil and their precursors recruited into bronchus membrane and to facilite the eosinophilic inflammation.