Abstract
Background: In CF airways, dysfunctional Cl– secretion and mucociliary clearance favor bacterial infections contributing to progressive lung damage and respiratory failure, the first cause of morbidity and mortality. We thus devote our efforts to identify novel therapeutic strategies to promote CF lung repair. We previously discovered that the capability of CF airway epithelia to repair is less efficient, than in healthy controls, due to the CFTR defect and bacterial infections, in particular with P. aeruginosa (PA) and S. aureus (SA). Our work also unveiled that CFTR modulators enhance airway repair, but both CFTR rescue and repair improvement are dampened by infection.
Published Version
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