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Edwards, M.R. et al.

Edwards, Mukaida, Johnson, Johnston,

IL-1beta induces IL-8 in bronchial cells via NF-kappaB and NF-IL6 transcription factors and can be suppressed by glucocorticoids.

IL-1beta may contribute to airway inflammation by inducing pro-inflammatory cytokines and chemokines from bronchial epithelial cells. In the current study, we investigated the cis-acting sites within the IL-8 promoter, and signalling pathways important in IL-8 production from BEAS2B cells following IL-1beta stimulation. IL-1beta treatment (0.1-10 ng/mL) upregulated IL-8 protein production in a dose dependent manner and IL-8 mRNA in a time dependent manner. IL-1beta induced upregulation of IL-8 promoter-reporter constructs, indicating that the mechanism of upregulation was pre-transcriptional. Using IL-8 promoter constructs with mutated cis-acting sites, it was found that both the NF-kappaB and NF-IL6 sites together were required for IL-8 promoter induction following IL-1beta treatment. Using chemical inhibitors or dominant negative mutants, we found that IL-8 promoter activity required IkappaB kinase beta, IkappaB, but not the MAP kinases p38 or c-Jun N-terminal kinase 2. Fluticasone propionate was able to suppress IL-1beta induced IL-8 protein and promoter activation, using both a -1481 bp fragment and a -133 bp fragment, indicating that the glucocorticoid response element found at -330 bp was not required for fluticasone mediated suppression of IL-8 promoter activation.[1]

References

IL-1beta induces IL-8 in bronchial cells via NF-kappaB and NF-IL6 transcription factors and can be suppressed by glucocorticoids. Edwards, M.R., Mukaida, N., Johnson, M., Johnston, S.L. Pulmonary pharmacology & therapeutics. (2005) [Pubmed]

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