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机构地区:[1]上海第二医科大学瑞金医院呼吸内科,上海200025 [2]上海第二医科大学瑞金医院上海消化外科研究所
出 处:《上海第二医科大学学报》2005年第7期694-697,共4页Acta Universitatis Medicinalis Secondae Shanghai
摘 要:目的以支气管上皮细胞株BEAS-2B细胞为研究对象,观察在Th2型细胞因子和促炎症因子肿瘤坏死因子-α(TNFα)的作用下,IL-8和IL-6的表达变化。方法通过RT-PCR方法测定Th2型细胞因子IL-4、IL-13以及促炎症因子TNFα单独和协同刺激下BEAS-2B细胞IL-8和IL-6的基因表达;通过ELISA方法测定细胞培养上清液中蛋白质的表达。结果在IL-4、IL-13和促炎症因子TNFα的单独刺激下,IL-6和IL-8的基因和蛋白质表达均较未刺激组显著增高;但IL-4、IL-13和TNFα协同刺激后,IL-8的基因和蛋白质表达进一步增高,而IL-6反而降低。结论支气管上皮细胞在TNFα和Th2型细胞因子的协同刺激下,通过调节IL-6和IL-8的表达,进一步调节嗜酸粒细胞性和非嗜酸粒细胞性炎症。ObjectiveIn order to evaluate Th2 cytokines and proinflammatory agents-TNFα on IL-6 and IL-8 production by bronchial epithelial cells.MethodsLevels of IL-6 and IL-8 mRNA and protein expressions in the bronchial epithelial cell line BEAS-2B cells were determined with RT-PCR and ELISA under the regulation of Th2 cytokine-IL-4,IL-13 with or without co-stimulation of TNFα.ResultsBoth IL-6 and IL-8 mRNA expressions tested by RT-PCR and protein levels tested by ELISA were significantly elevated under the stimulation of TNF-α and Th2 cytokines-IL-4 or IL-13 compared with the unstimulated control group. IL-4 and IL-13 had amplification effect on IL-8 gene expression and protein secretion when combined with TNFα. But they showed inhibitory effects both on IL-6 mRNA and protein production when co-stimulated with TNFα on the bronchial epithelial cells.ConclusionThis study demonstrates that Th2 cytokine and proinflammatory agents participate in the non-eosinophilic inflammatory process by regulating IL-6 and IL-8 expressions from bronchial epithelial cells.
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