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Impact of P.aeruginosa bacterial filtrate on CFTR channels and bronchial epithelial repair.
Author(s) -
Trinh Nguyen Thu Ngan,
Bilodeau Claudia,
Maillé Émilie,
Brochiero Emmanuelle
Publication year - 2013
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.27.1_supplement.1166.7
Subject(s) - cystic fibrosis , chemistry , airway , microbiology and biotechnology , lung , biology , medicine , surgery
Cystic fibrosis (CF) pathology, due to mutations in the CFTR, is characterized by bacterial colonisation and chronic inflammatory response leading to a progressive damage of the airways. It then becomes crucial to better understand the impact of these deleterious phenomena on the repair processes in attempt to restore the CF airways integrity. First, we confirmed, as in our previous studies, that the repair rates of airway epithelial CFBE‐ΔF508 (CF) monolayers were slower than that of CFBE‐wt (non‐CF) monolayers, which was, at least in part, dependent on CFTR function. We now observed that P. aeruginosa bacterial filtrate (PAF) inhibited wound closure of both non‐CF and CF CFBE monolayers. We also observed that wt‐ and ΔF508‐CFTR protein expressions, as well as Cl − currents through CFTR channels in CFBE‐wt monolayers were decreased after PAF exposure. Finally, CFTR corrector VRT‐325, initially developed to promote CFTR folding and function, was shown to be able to also improve the repair capacity of CF cell monolayers. However, its beneficial effect was abolished in the presence of PAF. This study showed that exoproducts from P. aeruginosa alter CFTR expression/function and also exhibit a deleterious effect on airway repair capacity, in basal condition or after CFTR correction. Project supported by Cystic Fibrosis Canada, the Canadian Lung Association, the CORAMH and Fondation Go.