CFTR Is a Negative Regulator of NFκB Mediated Innate Immune Response (original) (raw)
Figure 6
The CFTR knock out mice have elevated IκB-NFκB mediated inflammatory signaling.
The FABP-CFTR gut corrected CFTR knock-outs (CFKO) and wt- mice (n = 3) were injected i.p. with 15 mg/kg body weight of P. aeruginosa LPS or live bacteria (100 µl, 2×108), and IκB-p levels (24 hrs) were quantified by immunoblotting while serum IL1-β levels (6 or 24 hrs) were determined by ELISA. A. The representative immunoblot indicates the IκB-p protein levels in each group. The lung protein extracts of CFKO mice show inherent increase in IκB-p levels indicative of elevated NFκB signaling and activation. The densitometry analysis of IκB-p protein levels in CFKO lungs as compared to wild type mice show a 4.5 fold increase (n = 3, p<0.05) at baseline. B. The serum concentration of IL1-β (pg/ml) shown as mean±SD. The CFKO mice (red) have significantly higher pro-inflammatory cytokine, IL1-β, levels (***p<0.001 at 6 hrs while *p<0.05 at 24 hrs) on LPS induction as compared to wild type mice (green; **p<0.01).