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Cigarette Smoke Impairs Expression of the CFTR Chloride Channel in the Airways
Author(s) -
CormetBoyaka Estelle,
Hassan Fatemat,
Rennolds Jessica,
Nuovo Gerard,
Davis Ian C,
Diaz Philip,
Boyaka Prosper
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1039.31
Subject(s) - cystic fibrosis transmembrane conductance regulator , chloride channel , cystic fibrosis , lung , chemistry , cigarette smoke , inflammation , airway , immunohistochemistry , immunology , medicine , biology , biochemistry , toxicology , anesthesia
The Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a chloride channel that resides in the apical membrane of airway epithelial cells. Decreased CFTR expression or function leads to impaired regulation of the airway surface volume and composition resulting in altered clearance of bacteria, chronic infection and inflammation. We investigated whether cigarette smoke affected the expression and function of the CFTR chloride channel in the airways. When the human bronchial epithelial cells Calu‐3 were exposed to cigarette smoke extracts from Camel cigarettes, we observed reduced CFTR expression. This suppression occurred in a time‐ and dose‐dependent manner and was observed both at the mRNA and protein levels. Similarly, mice treated nasally with cigarette smoke extracts exhibited an inhibition of the CFTR activity. Finally, we analyzed CFTR expression in human lung samples by immunohistochemistry. In these assays, lung samples from smokers exhibit reduced CFTR protein expression, mostly in bronchial epithelial cells. Together, our results show that cigarette smoke regulates the expression and function of the CFTR chloride channel. Due to the critical role played by CFTR in the lung, future studies should investigate the role of CFTR in cigarette smoke related diseases.