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[Effects of NF-kappaB on the expression of IL-8 in human bronchial epithelial cells induced by cigarette smoke condensates].

OBJECTIVE
To investigate the effects of NF-kappaB on the expression of IL-8 in human bronchial epithelial cells induced by cigarette smoke condensates (CSC).


METHODS
Both IL-8mNF-kappaB(-) BEAS-2B cells (BEAS-2B cells with mutated NF-kappaB binding site in IL-8 promoter) and IL-8 WT BEAS-2B cells (wild-type BEAS-2B cells with completed NF-kappaB 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-kappaB(-) BEAS-2B cells (P < 0.001), the mRNA level of fLCF in IL-8 WT BEAS-2B cells was 1.32 times as that in IL-8mNF-kappaB(-) BEAS-2B cells (P < 0.001).


CONCLUSION
The results suggested that NF-kappaB 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.