in chronic rhinosinusitis: the effect on the epithelial chloride channel (cystic fibrosis transmembrane conductance regulator, CFTR) and the epithelial sodium channel (ENaC) physiology.

Chronic rhinosinusitis (CRS) is an inflammatory disease of the nose and the paranasal sinuses, often associated with an infection by . Disturbance in the function of ion channels is regarded as an etiological factor for pathogenesis of CRS. The study aims to measure the mRNA expression of the ENaC and CFTR ion channels in nasal epithelial cells (NECs) and to investigate the effect of both the budesonide and on these ion channels. NECs biopsies obtained from healthy volunteers and patients with CRS. NECs were infected with strains and/or budesonide to study the mRNA expression levels of the ENaC and CFTR ion channels. The mRNA expression level of CFTR was increased while that of ENaC was decreased infection and budesonide treatment induced a significant modulation of ENaC and CFTR ion channels expression. The CFTR and ENaC ion channel physiology are of importance in the pathogenesis of CRS. Exposure to infection and treatment with budesonide modulated the mRNA expression of CFTR and ENaC ion channels. Better understanding of the pathophysiology of CRS.