白介素5受体α链在支气管上皮细胞的表达

IL-5 receptor expression on bronchial epithelial cell

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 We investigated both IL-5Rαgene 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 cell was investigated after stimulated by TNF-α,IL-5,IL-4,IL-13 and LTC4.RT-PCR was used to evaluate IL-5Rαgene expression and flow cytometry was used to assess IL-5Rαprotein expression.We also investigate BEAS-2B cell on ICAM-1,VCAM-1 and IL-5Rαcoordinate expression under the stimulation of TNF-αand IL-5.Results Th2 cytokines and leukotriene C4 that can stimulate BEAS-2B cell express IL-5Rα gene in some extent.Those groups stimulated by TNF-αalone or TNF-αcombine with other cytokines strongly expressed IL-5Rαgene.Detected by flow cytometry,BEAS-2B cell stimulated by TNF-αalone or combine with other cytokines for 16 hours can express IL-5Rαprotein compare to unstimulated cells or stimulated with Th2 cytokines and LTC4 alone.Along with the stimulation time,IL-5Rαprotein expression decreased.Both VCAM-1 and IL-5Rαprotein expression elevated by the stimulation of TNF-αcombination with IL-5,while ICAM-1 were consecutively expressed on bronchial epithelial cell.Conclusions We found in our study that IL-5Rαgene and protein were expressed on BEAS-2B cell under the stimulation of inflammatory agents.IL-5 and TNF-αcan increase bronchial epithelial cell express IL-5Rαand adhesion molecule-VCAM-1,then.attract eosinophil and their precursors recruiting into the bronchus membrane and push forward the eosinophilic inflammation.