Effect of Electronic Cigarette Vapour Exposure on Ca(2+)- and cAMP-Dependent Ion Transport in Human Airway Epithelial Cells.

PURPOSE: The popularity of electronic cigarettes (e-cigarettes) has grown exponentially over the past few years, and teenagers now prefer them to tobacco cigarettes. We determined whether exposure to e-cigarette vapour (e-vapour) adversely affects ion transport using human airway epithelial cell lines 16HBE14o- and Calu-3 and well-differentiated primary human bronchial epithelial cells (HBEs). METHODS: We concurrently measured fluorescent signals and short-circuit current (I(SC)), an indicator of electrogenic ion transport, in polarised epithelia. The P2Y receptor-mediated signalling pathway was used to induce an increase in intracellular calcium concentration ([Ca(2+)](i)) and I(SC). We used a single-polypeptide fluorescence resonance energy transfer reporter based on exchange proteins directly activated by cAMP (Epac) to measure forskolin-induced changes in cAMP and I(SC). RESULTS: We compared the effects of e-vapour to those of traditional cigarette smoke (CS) on the human airway cell models. In all three cell types, e-vapour, similar to CS, significantly reduced agonist-induced increases in Ca(2+) or cAMP signalling and I(SC). However, reductions in the epithelial electrolyte transport activities did not correlate with any changes in the protein levels of various ion channels and transporters. CONCLUSION: Our data suggest that e-vapour is not harmless and causes ion transport dysfunction similar to CS, thereby predisposing e-cigarette users to vaping-induced lung injury.