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Decreases or loss of channel function often lead to mucus stasis, chronic bacterial infections, and the accompanying chronic inflammatory responses that promote progressive lung destruction, and, eventually in CF, lung failure. Here we discuss CFTR's functional role airway surface liquid hydration and pH, in regulation of other channels such as the epithelial sodium channel, and in regulating inflammatory responses in the lung.<\/jats:p>","DOI":"10.1152\/ajplung.00326.2014","type":"journal-article","created":{"date-parts":[[2014,11,8]],"date-time":"2014-11-08T07:18:57Z","timestamp":1415431137000},"page":"L917-L923","source":"Crossref","is-referenced-by-count":83,"title":["CFTR and lung homeostasis"],"prefix":"10.1152","volume":"307","author":[{"given":"James F.","family":"Collawn","sequence":"first","affiliation":[{"name":"Department of Cell, Developmental and Integrative Biology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;"},{"name":"Pulmonary Injury and Repair Center, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and"},{"name":"Gregory Fleming James Cystic Fibrosis Center, School of Medicine, University of Alabama at Birmingham, Birmingham, 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