AbstractCystic fibrosis (CF) is a hereditary disease caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The lung disease is, however, also associated with dysregulation of the epithelial sodium channel (ENaC) which leads to dehydrated airways predisposing the individual to chronic cycles of infection and inflammation. ENaC is activated by trypsin-like channel activating proteases (TLPs), inhibition of which increases airway surface liquid volume and improves mucociliary function of primary human airway epithelial cells (hAECs) grown at air-liquid interface (ALI).
Thesis is embargoed until 31 December 2027.
|Date of Award||Dec 2022|
|Supervisor||Lorraine Martin (Supervisor), Damian Downey (Supervisor) & James Reihill (Supervisor)|
- cystic fibrosis
- epithelial sodium channel