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dc.contributor.authorDonovan, C
dc.contributor.authorSeow, HJ
dc.contributor.authorBourke, JE
dc.contributor.authorVlahos, R
dc.date.accessioned2021-02-05T01:23:07Z
dc.date.available2021-02-05T01:23:07Z
dc.date.issued2016-05-01
dc.identifierpii: CS20160093
dc.identifier.citationDonovan, C., Seow, H. J., Bourke, J. E. & Vlahos, R. (2016). Influenza A virus infection and cigarette smoke impair bronchodilator responsiveness to beta-adrenoceptor agonists in mouse lung. CLINICAL SCIENCE, 130 (10), pp.829-837. https://doi.org/10.1042/CS20160093.
dc.identifier.issn0143-5221
dc.identifier.urihttp://hdl.handle.net/11343/260377
dc.description.abstractβ2-adrenoceptor agonists are the mainstay therapy for patients with asthma but their effectiveness in cigarette smoke (CS)-induced lung disease such as chronic obstructive pulmonary disease (COPD) is limited. In addition, bronchodilator efficacy of β2-adrenoceptor agonists is decreased during acute exacerbations of COPD (AECOPD), caused by respiratory viruses including influenza A. Therefore, the aim of the present study was to assess the effects of the β2-adrenoceptor agonist salbutamol (SALB) on small airway reactivity using mouse precision cut lung slices (PCLS) prepared from CS-exposed mice and from CS-exposed mice treated with influenza A virus (Mem71, H3N1). CS exposure alone reduced SALB potency and efficacy associated with decreased β2-adrenoceptor mRNA expression, and increased tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β) expression. This impaired relaxation was restored by day 12 in the absence of further CS exposure. In PCLS prepared after Mem71 infection alone, responses to SALB were transient and were not well maintained. CS exposure prior to Mem71 infection almost completely abolished relaxation, although β2-adrenoceptor and TNFα and IL-1β expression were unaltered. The present study has shown decreased sensitivity to SALB after CS or a combination of CS and Mem71 occurs by different mechanisms. In addition, the PCLS technique and our models of CS and influenza infection provide a novel setting for assessment of alternative bronchodilators.
dc.languageEnglish
dc.publisherPORTLAND PRESS LTD
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleInfluenza A virus infection and cigarette smoke impair bronchodilator responsiveness to beta-adrenoceptor agonists in mouse lung
dc.typeJournal Article
dc.identifier.doi10.1042/CS20160093
melbourne.affiliation.departmentPharmacology and Therapeutics
melbourne.affiliation.departmentBiochemistry and Molecular Biology
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titleClinical Science
melbourne.source.volume130
melbourne.source.issue10
melbourne.source.pages829-837
melbourne.identifier.nhmrc1027112
melbourne.identifier.nhmrc1041575
dc.rights.licenseCC BY
melbourne.elementsid1057264
melbourne.contributor.authorBOURKE, JANE
melbourne.contributor.authorVlahos, Ross
melbourne.contributor.authorDONOVAN, CHANTAL
melbourne.contributor.authorSEOW, HUEI
dc.identifier.eissn1470-8736
melbourne.identifier.fundernameidNHMRC, 1027112
melbourne.identifier.fundernameidNHMRC, 1041575
melbourne.accessrightsOpen Access


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