The epithelial sodium channel ENaC consists of three subunits encoded by Scnn1a, Scnn1b, and Scnn1g and increased sodium absorption through this channel is hypothesized to lead to mucus dehydration and accumulation in cystic fibrosis (CF) patients.
To address these questions, Scnn1b-Tg mice, which exhibit airway mucus dehydration/adhesion, were compared and crossed with Muc5b- and Muc5ac-deficient mice.
Scnn1b-Tg mice, which exhibit chronic airway surface dehydration from birth, can be used as a model to study the pathogenesis of muco-obstructive lung disease across developmental stages.