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dc.contributor.author Omar, Shadia
dc.contributor.author Clarke, Rebecca
dc.contributor.author Abdullah, Haniah
dc.contributor.author Brady, Clare
dc.contributor.author Corry, John
dc.contributor.author Winter, Hanagh
dc.contributor.author Touzelet, Olivier
dc.contributor.author Power, Ultan F.
dc.contributor.author Lundy, Fionnuala
dc.contributor.author McGarvey, Lorcan P. A.
dc.contributor.author Cosby, S. Louise
dc.date.accessioned 2017-02-17T18:19:16Z
dc.date.available 2017-02-17T18:19:16Z
dc.date.issued 2017-02-10
dc.identifier doi:10.5061/dryad.p170v
dc.identifier.citation Omar S, Clarke R, Abdullah H, Brady C, Corry J, Winter H, Touzelet O, Power UF, Lundy F, McGarvey LPA, Cosby SL (2017) Respiratory virus infection up-regulates TRPV1, TRPA1 and ASICS3 receptors on airway cells. PLOS ONE 12(2): e0171681.
dc.identifier.issn 1932-6203
dc.identifier.uri http://hdl.handle.net/10255/dryad.137117
dc.description Receptors implicated in cough hypersensitivity are transient receptor potential vanilloid 1 (TRPV1), transient receptor potential cation channel, Subfamily A, Member 1 (TRPA1) and acid sensing ion channel receptor 3 (ASIC3). Respiratory viruses, such as respiratory syncytial virus (RSV) and measles virus (MV) may interact directly and/or indirectly with these receptors on sensory nerves and epithelial cells in the airways. We used in vitro models of sensory neurones (SHSY5Y or differentiated IMR-32 cells) and human bronchial epithelium (BEAS-2B cells) as well as primary human bronchial epithelial cells (PBEC) to study the effect of MV and RSV infection on receptor expression. Receptor mRNA and protein levels were examined by qPCR and flow cytometry, respectively, following infection or treatment with UV inactivated virus, virus-induced soluble factors or pelleted virus. Concentrations of a range of cytokines in resultant BEAS-2B and PBEC supernatants were determined by ELISA. Up-regulation of TRPV1, TRPA1 and ASICS3 expression occurred by 12 hours post-infection in each cell type. This was independent of replicating virus, within the same cell, as virus-induced soluble factors alone were sufficient to increase channel expression. IL-8 and IL-6 increased in infected cell supernatants. Antibodies against these factors inhibited TRP receptor up-regulation. Capsazepine treatment inhibited virus induced up-regulation of TRPV1 indicating that these receptors are targets for treating virus-induced cough.
dc.relation.haspart doi:10.5061/dryad.p170v/1
dc.relation.isreferencedby doi:10.1371/journal.pone.0171681
dc.subject Respiratory viruses
dc.subject TRPV1
dc.subject TRPA1
dc.subject ASICS 3
dc.subject Cough
dc.subject asthma
dc.subject COPD
dc.subject Measles virus
dc.subject Respiratory syncytial virus
dc.title Data from: Respiratory virus infection up-regulates TRPV1, TRPA1 and ASICS3 receptors on airway cells
dc.type Article
dc.contributor.correspondingAuthor Cosby, Sara
prism.publicationName PLOS ONE

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