Expression of wild-type CFTR suppresses NF-kappaB-driven inflammatory signalling.

PloS One
Mairi J HunterAnil Mehta

Abstract

Mutation of the cystic fibrosis transmembrane-conductance regulator (CFTR) causes cystic fibrosis (CF) but not all CF aspects can easily be explained by deficient ion transport. CF-inflammation provides one example but its pathogenesis remains controversial. Here, we tested the simple but fundamental hypothesis that wild-type CFTR is needed to suppress NF-kappaB activity. In lung epithelial (H441) and engineered (H57) cell lines; we report that inflammatory markers are significantly suppressed by wild-type CFTR. Transient-transfection of wild-type CFTR into CFTR-naïve H441 cells, dose-dependently down-regulates both basal and Tumour Necrosis Factor-alpha evoked NF-kappaB activity when compared to transfection with empty vector alone (p<0.01, n>5). This effect was also observed in CFTR-naïve H57-HeLa cells which stably express a reporter of NF-kappaB activity, confirming that the CFTR-mediated repression of inflammation was not due to variable reporter gene transfection efficiency. In contrast, H57 cells transfected with a control cyano-fluorescent protein show a significantly elevated basal level of NF-kappaB activity above control. Initial cell seeding density may be a critical factor in mediating the suppressive effects of CF...Continue Reading

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Citations

Jun 17, 2014·Life Sciences·Leticia Cristina Radin PereiraTânia Silvia Fröde
May 25, 2011·Naunyn-Schmiedeberg's Archives of Pharmacology·Andrea VenerandoAnil Mehta
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May 4, 2021·Frontiers in Pharmacology·Lisa KünziStefanie Krick

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Methods Mentioned

BETA
bronchoalveolar
lavage
transfection
transfecting
ELISA
PCR
transfections
ELISAs

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