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Goblet Cell Hyperplasia Requires High Bicarbonate Transport To Support Mucin Release.

Scientific reports (2016-10-28)
Giulia Gorrieri, Paolo Scudieri, Emanuela Caci, Marco Schiavon, Valeria Tomati, Francesco Sirci, Francesco Napolitano, Diego Carrella, Ambra Gianotti, Ilaria Musante, Maria Favia, Valeria Casavola, Lorenzo Guerra, Federico Rea, Roberto Ravazzolo, Diego Di Bernardo, Luis J V Galietta
ABSTRACT

Goblet cell hyperplasia, a feature of asthma and other respiratory diseases, is driven by the Th-2 cytokines IL-4 and IL-13. In human bronchial epithelial cells, we find that IL-4 induces the expression of many genes coding for ion channels and transporters, including TMEM16A, SLC26A4, SLC12A2, and ATP12A. At the functional level, we find that IL-4 enhances calcium- and cAMP-activated chloride/bicarbonate secretion, resulting in high bicarbonate concentration and alkaline pH in the fluid covering the apical surface of epithelia. Importantly, mucin release, elicited by purinergic stimulation, requires the presence of bicarbonate in the basolateral solution and is defective in cells derived from cystic fibrosis patients. In conclusion, our results suggest that Th-2 cytokines induce a profound change in expression and function in multiple ion channels and transporters that results in enhanced bicarbonate transport ability. This change is required as an important mechanism to favor release and clearance of mucus.

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Sigma-Aldrich
Anti-SLC12A2 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

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