CFTR Is a Negative Regulator of NFκB Mediated Innate Immune Response (original) (raw)
Figure 3
Inhibition of CFTR regulated NFκB signaling under conditions that disrupt lipid rafts.
CFBE41o- cells stably transduced with wt-CFTR were transiently transfected with IL-8 or NFκB reporter constructs and a renila luciferase internal control plasmid (n = 3). The cells were induced with 1 ng/ml IL1-β and/or treated with 5 mM methyl-β-cyclodextrin (CD) for 6 hrs (A), and/or 10 µM CFTR-172 inhibitor overnight (B). The data are shown as mean±SD of IL-8 or NFκB promoter activities normalized to renila luciferase internal control. A. IL-1β induced IL-8 and NFκB promoter driven luciferase expression, and wt-CFTR dampened baseline and cytokine induced reporter activity (Figs 1&2). Pre-treatment with CD under conditions known to disrupt lipid rafts eliminated the effect of wt-CFTR, *p<0.05. B. Cells were transfected as in A but instead of treatment with CD, the CFTR-172 inhibitor was included to block CFTR-mediated chloride secretion at the plasma membrane. Pre-treatment with CFTR 172 inhibitor induced IL-8 and NFκB promoter activities and eliminated the inhibitory effect of wt-CFTR, *p<0.05.