The Effect of Sodium Bicarbonate, a Beneficial Adjuvant Molecule in Cystic Fibrosis,
on Bronchial Epithelial Cells Expressing a Wild-Type or Mutant CFTR Channel
Clinical and experimental results with inhaled sodium bicarbonate as an adjuvant therapy
in cystic fibrosis (CF) are promising due to its mucolytic and bacteriostatic properties,
but its direct effect has not been studied on respiratory epithelial cells. Our aim
was to establish and characterize co-culture models of human CF bronchial epithelial
(CFBE) cell lines expressing a wild-type (WT) or mutant (deltaF508) CF transmembrane
conductance regulator (CFTR) channel with human vascular endothelial cells and investigate
the effects of bicarbonate. Vascular endothelial cells induced better barrier properties
in CFBE cells as reflected by the higher resistance and lower permeability values.
Activation of CFTR by cAMP decreased the electrical resistance in WT but not in mutant
CFBE cell layers confirming the presence and absence of functional channels, respectively.
Sodium bicarbonate (100 mM) was well-tolerated by CFBE cells: it slightly reduced
the impedance of WT but not that of the mutant CFBE cells. Sodium bicarbonate significantly
decreased the more-alkaline intracellular pH of the mutant CFBE cells, while the barrier
properties of the models were only minimally changed. These observations indicate
that sodium bicarbonate is beneficial to deltaF508-CFTR expressing CFBE cells. Thus,
sodium bicarbonate may have a direct therapeutic effect on the bronchial epithelium.