NF-κB在香烟烟雾凝集物诱导人支气管上皮细胞IL-8表达中的作用

Effects of NF-κB on the expression of IL-8 in human bronchial epithelial cells induced by cigarette smoke condensates

目的研究核因子κB(NF-κB)在香烟烟雾凝集物(CSC)诱导人支气管上皮细胞IL-8表达中的作用。方法利用IL-8促进子上NF-κB结合位点突变的BEAS-2B细胞株(IL-8mNF-κB-BEAS-2B细胞)和野生型BEAS-2B细胞株(IL-8 WT BEAS-2B细胞,其IL-8促进子上含有完整的NF-κB结合位点),经7.5%CSC处理后,用荧光定量PCR方法检测处理后细胞荧光素酶基因(luciferase,fLCF)mRNA水平的变化,并用荧光素酶报告基因活性检测试剂盒检测处理后细胞的荧光素酶活性大小。结果 7.5%CSC处理2种BEAS-2B细胞后,IL-8 WT BEAS-2B细胞的fLCF mRNA表达量和荧光素酶活性均高于IL-8mNF-κB-BEAS-2B细胞(P<0.001),其中fLCF mRNA表达量是IL-8mNF-κB-BEAS-2B细胞的1.32倍(P<0.001)。结论 NF-κB转录因子通过参与炎症因子IL-8表达,促进吸烟导致的呼吸系统炎症反应。

Objective To investigate the effects of NF-κB on the expression of IL-8 in human bronchial epithelial cells induced by cigarette smoke condensates（CSC）.Methods Both IL-8mNF-κB-BEAS-2B cells（BEAS-2B cells with mutated NF-κB binding site in IL-8 promoter） and IL-8 WT BEAS-2B cells（wild-type BEAS-2B cells with completed NF-κB binding site in IL-8 promoter） were treated by 7.5% CSC.The mRNA level of fLCF gene was detected by real-time PCR,and the activity of luciferase was measured by luciferase reporter gene activity detection kit.Results After two kinds of BEAS-2B cells were treated by 7.5% CSC,the mRNA level of fLCF and the activity of luciferase in IL-8 WT BEAS-2B cells was higher than those in IL-8mNF-κB-BEAS-2B cells（P0.001）,the mRNA level of fLCF in IL-8 WT BEAS-2B cells was 1.32 times as that in IL-8mNF-κB-BEAS-2B cells（P0.001）.Conclusion The results suggested that NF-κB transcription factor was involved in smoking-induced respiratory inflammation through the precise molecular mechanisms of promoting the release of IL-8 in BEAS-2B cells treated by CSC.