Marked increases in mucociliary clearance produced by synergistic secretory agonists or inhibition of the epithelial sodium channel.

ABSTRACT: Mucociliary clearance (MCC) is a critical host innate defense mechanism in airways, and it is impaired in cystic fibrosis (CF) and other obstructive lung diseases. Epithelial fluid secretion and absorption modify MCC velocity (MCCV). We tested the hypotheses that inhibiting fluid absorption accelerates MCCV, whereas inhibiting fluid secretion decelerates it. In airways, ENaC is mainly responsible for fluid absorption, while anion channels, including CFTR and Ca²⁺-activated chloride channels mediate anion/fluid secretion. MCCV was increased by the cAMP-elevating agonists, forskolin or isoproterenol (10 μM) and by the Ca²⁺-elevating agonist, carbachol (0.3 μM). The CFTR-selective inhibitor, CFTR_inh-172, modestly reduced MCCV-increases induced by forskolin or

SUBMITTER: Joo NS 

PROVIDER: S-EPMC5103292 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature