Inhibitory effects of PAR2 activating peptides and analogues on influenza A infection in mice

Richard Betts

    Research output: ThesisDoctoral Thesis

    24 Downloads (Pure)


    [Truncated] Respiratory tract infections caused by influenza A viruses are associated with considerable morbidity and mortality throughout the world. Furthermore, influenza A viral infections can exacerbate pre-existing asthma and induce several hallmark features of the condition, including airways inflammation and airways hyperresponsiveness i:n otherwise healthy individuals. As a result, murine models of influenza A infection are a valuable and frequently used platform for examining potential modulators of respiratory tract inflammatory processes, such as protease-activated receptors (PARs). PARs are 7- transmembrane domain, G-protein coupled receptors that act as sensors of extracellular proteolytic activity. PAR activation typically involves the cleavage of a specific site within the extracellular N-terminal region of the receptor, which generates a newly formed tethered ligand sequence that interacts with the 2nd extracellular loop of the receptor to confer cellular signalling. Activation of a particular PAR isoform, P AR2, has previously been shown to be beneficial in various models of inflammatory airway disease, although the effect of P AR2 activation in virus-induced models of airways inflammation has not been determined. Thus, this thesis set out to examine the effect of P AR2 activators on inflammatory events within a murine model of influenza A virus­induced airways inflammation.
    Original languageEnglish
    QualificationDoctor of Philosophy
    Awarding Institution
    • The University of Western Australia
    Publication statusUnpublished - 2007

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    This thesis has been made available in the UWA Profiles and Research Repository as part of a UWA Library project to digitise and make available theses completed before 2003. If you are the author of this thesis and would like it removed from the UWA Profiles and Research Repository, please contact


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