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Please use this identifier to cite or link to this item: http://hdl.handle.net/10373/384

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Title: Cation currents in human airway epithelial cells induced by infection with influenza A virus
Authors: Gallacher, M.
Brown, Sean G.
Hale, B. G.
Fearns, R.
Olver, R. E.
Randall, R. E.
Wilson, S. M.
Affiliation: University of Abertay Dundee. School of Contemporary Sciences
Keywords: Influenza
Issue Date: 1-Jul-2009
Publisher: Wiley-Blackwell
Type: Journal Article
Refereed: peer-reviewed
Rights: Published version (c)Wiley-Blackwell, available from DOI: 10.1113/jphysiol.2009.171223. The definitive version is available at www3.interscience.wiley.com
Citation: Gallacher, M., et al. 2009. Cation currents in human airway epithelial cells induced by infection with influenza A virus. Journal of Physiology. 587(13): pp.3159-3173. Available at DOI: 10.1113/jphysiol.2009.171223
Abstract: Influenza A viruses cause lung disease via an incompletely understood mechanism that involves the accumulation of liquid within the lungs. The accumulation of lung liquid is normally prevented by epithelial Na(+) absorption, a transport process regulated via several pathways including phosphoinositide-3-kinase (PI3K). Since the influenza A virus encodes a non-structural protein (NS1) that can activate this kinase, we now explore the effects of NS1 upon the biophysical properties of human airway epithelial cells. Transient expression of NS1 depolarized electrically isolated cells maintained in glucocorticoid-free medium by activating a cation conductance identical to the glucocorticoid-induced conductance seen in single cells. This response involved PI3K-independent and PI3K-dependent mechanisms. Infecting glucocorticoid-deprived cells with influenza A virus disrupted the normal electrical coupling between neighbouring cells, but also activated a conductance identical to that induced by NS1. This response to virus infection was only partially dependent upon NS1-mediated activation of PI3K. The presence of NS1 allows influenza A to modify the biophysical properties of infected cells by activating a Na(+)-permeable conductance. Whilst the activation of Na(+)-permeable channels may be expected to increase the rate of Na(+) absorption and thus reduce the volume of liquid in the lung, liquid does normally accumulate in influenza A-infected lungs. The overall effect of influenza A on lung liquid volume may therefore reflect a balance between the activation and inhibition of Na(+)-permeable channels.
URI: http://hdl.handle.net/10373/384
ISSN: 0022-3751
Appears in Collections:Science Engineering & Technology Collection

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