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- W63993757 abstract "Mutations of CFTR results in defective Cl− secretion and Na+ hyperabsorption which contributes to a reduction of the airway surface liquid layer height (ASLh) thus promoting bacterial colonization and inflammation. Lipoxin A4 (LXA4) which plays a central role in resolving inflammation is decreased in cystic fibrosis (CF). We have investigated the role of LXA4 in modulating ion transport and ASLh in CF and non-CF bronchial epithelial cell lines (CuFi-1 and Nuli-1) and primary cultures grown under an air-liquid interface. ASLh were measured using confocal microscopy and ion transport using electrophysiological techniques. LXA4 (1nM) significantly increased ASLh in CF and non-CF epithelia. This effect was inhibited by bumetanide, amiloride, Boc-2 (FPR2 antagonist), extracellular hexokinase, reactive blue 2 and NF340 (P2Y and P2Y11 receptor antagonist). LXA4 stimulated a carbenoxolone (Panexin-1 inhibitor)-sensitive apical ATP release, intracellular Ca2+ mobilization and Cl− secretion and inhibited Na+ absorption. These effects of LXA4 involving apical ATP release, inhibition of Na+ absorption and stimulation of Cl− secretion to enhance ASL dynamics open up a new therapeutic avenue to promote mucociliary clearance in CF airways." @default.
- W63993757 created "2016-06-24" @default.
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- W63993757 date "2012-04-01" @default.
- W63993757 modified "2023-09-23" @default.
- W63993757 title "Regulation of ion transport and ASL height by the anti‐inflammatory mediator, lipoxin A4 in normal and cystic fibrosis bronchial epithelium" @default.
- W63993757 doi "https://doi.org/10.1096/fasebj.26.1_supplement.696.9" @default.
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