Abstract
The life-shortening genetic disease cystic fibrosis (CF) is caused by mutations in the CF gene on both alleles, resulting in failure of a defective CF transmembrane conductance regulator (CFTR) glycoprotein to normally regulate chloride and bicarbonate flux at the airway surface.1 According to a leading theory of CF pathogenesis, the “volume depletion” hypothesis, this abnormal anion transport leads to reduced airway surface liquid, airway dehydration, and impaired mucociliary clearance, resulting in vulnerability to airway obstruction, microbial infection, and inflammation.
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