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HCO 3  −  secretion in distal airways is critical for airway mucosal defense. HCO 3  − /H +  transport across the apical membrane of airway surface epithelial cells was studied by measuring intracellular pH in luminally microperfused freshly dissected mice bronchioles. Functional studies demonstrated that CFTR, ENaC, Cl − –HCO 3  −  exchange, Na + -H +  exchange, and Na + –HCO 3  −  cotransport are involved in apical HCO 3  − /H +  transport. RT-PCR of isolated bronchioles detected fragments from Cftr, α, β, γ subunits of ENaC, Ae2, Ae3, NBCe1, NBCe2, NBCn1, NDCBE, NBCn2, Nhe1, Nhe2, Nhe4, Nhe5, Slc26a4, Slc26a6, and Slc26a9. We assume that continuous decline of intracellular pH following alkaline load demonstrates time course of HCO 3  −  secretion into the lumen which is perfused with a HCO 3  − -free solution. Forskolin-stimulated HCO 3  −  secretion was substantially inhibited by luminal application of CFTR inh -172 (5 μM), H 2 DIDS (200 μM), and amiloride (1 μM). In bronchioles from a cystic fibrosis mouse model, basal and acetylcholine-stimulated HCO 3  −  secretion was substantially impaired, but forskolin transiently accelerated HCO 3  −  secretion of which the magnitude was comparable to wild-type bronchioles. In conclusion, we have characterized apical HCO 3  − /H +  transport in native bronchioles. We have demonstrated that cAMP-mediated and Ca 2+ -mediated pathways are involved in HCO 3  −  secretion and that apical HCO 3  −  secretion is largely mediated by CFTR and H 2 DIDS-sensitive Cl − –HCO 3  −  exchanger, most likely Slc26a9. The impairment of HCO 3  −  secretion in bronchioles from a cystic fibrosis mouse model may be related to the pathogenesis of early lung disease in cystic fibrosis.

Bicarbonate transport of airway surface epithelia in luminally perfused mice bronchioles