Accordingly, taken together with previous studies on Cif, the data in this paper are consistent with the view that Cif-mediated reductions in CFTR abundance (∼60%) and chloride secretion (∼60%) by human airway epithelial cells [4] would be expected to reduce mucociliary clearance in the airway, a critical mechanism of the innate immune response to eliminate P. aeruginosa and other pathogens from the airway of patients with COPD, ventilator-associated pneumonia, CF and bronchiectasis [42], [43]. This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.