id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-000609-dpcgl6ig	Raju, Sammeta V.	Suppression of Adenosine-Activated Chloride Transport by Ethanol in Airway Epithelia	2012-03-19		.txt	text/plain	4083	253	43	Here, air-liquid interface cultures of Calu-3 epithelial cells were basolaterally exposed to physiologically relevant concentrations of ethanol (0, 25, 50 and 100 mM) for 24 hours and adenosine-stimulated ion transport was measured by Ussing chamber. These results imply that ethanol exposure dysregulates CFTR-mediated chloride transport in airways by suppression of adenosine-A(2B)AR-cAMP signaling pathway, which might contribute to alcohol-associated lung infections. The current report directly measured the adenosineinduced chloride secretion of airway epithelia under the exposure of physiologically relevant concentrations of alcohol and found that ethanol attenuates epithelial CFTR-mediated chloride transport by modulating cellular cAMP levels. To explore if ethanol affects adenosine-activated ion transport function of airway epithelium, we employed air-liquid interface cultures of Calu-3 cells, a system widely used to investigate airway epithelial electrophysiological properties [27, 28] . These results not only confirm that ethanol modulates adenosine-cAMP signaling but also suggest that phosphodiesterase inhibitors may be useful as the potential therapeutic agents for improving the airway epithelial ion transport and mucociliary clearance in alcoholic patients.	./cache/cord-000609-dpcgl6ig.txt	./txt/cord-000609-dpcgl6ig.txt