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  • JOURNAL ARTICLE
    Belvisi MG, Birrell MA, Khalid S, Wortley MA, Dockry R, Coote J, Holt K, Dubuis E, Kelsall A, Maher SA, Bonvini S, Woodcock A, Smith JAet al., 2016,

    Neurophenotypes in Airway Diseases Insights from Translational Cough Studies

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 193, Pages: 1364-1372, ISSN: 1073-449X
  • JOURNAL ARTICLE
    Bonvini SJ, Birrell MA, Grace MS, Maher SA, Adcock JJ, Wortley MA, Dubuis E, Ching Y-M, Ford AP, Shala F, Miralpeix M, Tarrason G, Smith JA, Belvisi MGet al., 2016,

    Transient receptor potential cation channel, subfamily V, member 4 and airway sensory afferent activation: Role of adenosine triphosphate

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 138, Pages: 249-+, ISSN: 0091-6749
  • JOURNAL ARTICLE
    Birrell MA, Maher SA, Dekkak B, Jones V, Wong S, Brook P, Belvisi MGet al., 2015,

    Anti-inflammatory effects of PGE(2) in the lung: role of the EP4 receptor subtype

    , Thorax, Vol: 70, Pages: 740-747, ISSN: 0040-6376

    Background Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the airway. Current treatment options (long acting β-adrenoceptor agonists and glucocorticosteroids) are not optimal as they are only effective in certain patient groups and safety concerns exist regarding both compound classes. Therefore, novel bronchodilator and anti-inflammatory strategies are being pursued. Prostaglandin E2 (PGE2) is an arachidonic acid-derived eicosanoid produced by the lung which acts on four different G-protein coupled receptors (EP1–4) to cause an array of beneficial and deleterious effects. The aim of this study was to identify the EP receptor mediating the anti-inflammatory actions of PGE2 in the lung using a range of cell-based assays and in vivo models.Methods and results It was demonstrated in three distinct model systems (innate stimulus, lipopolysaccharide (LPS); allergic response, ovalbumin (OVA); inhaled pollutant, cigarette smoke) that mice missing functional EP4 (Ptger4−/−) receptors had higher levels of airway inflammation, suggesting that endogenous PGE2 was suppressing inflammation via EP4 receptor activation. Cell-based assay systems (murine and human monocytes/alveolar macrophages) demonstrated that PGE2 inhibited cytokine release from LPS-stimulated cells and that this was mimicked by an EP4 (but not EP1–3) receptor agonist and inhibited by an EP4 receptor antagonist. The anti-inflammatory effect occurred at the transcriptional level and was via the adenylyl cyclase/cAMP/ cAMP-dependent protein kinase (PKA) axis.Conclusion This study demonstrates that EP4 receptor activation is responsible for the anti-inflammatory activity of PGE2 in a range of disease relevant models and, as such, could represent a novel therapeutic target for chronic airway inflammatory conditions.

  • JOURNAL ARTICLE
    Baxter M, Eltom S, Dekkak B, Yew-Booth L, Dubuis ED, Maher SA, Belvisi MG, Birrell MAet al., 2014,

    Role of transient receptor potential and pannexin channels in cigarette smoke-triggered ATP release in the lung

    , THORAX, Vol: 69, Pages: 1080-1089, ISSN: 0040-6376
  • JOURNAL ARTICLE
    Raemdonck K, de Alba J, Birrell MA, Grace M, Maher SA, Irvin CG, Fozard JR, O'Byrne PM, Belvisi MGet al., 2012,

    A role for sensory nerves in the late asthmatic response

    , THORAX, Vol: 67, Pages: 19-25, ISSN: 0040-6376
  • JOURNAL ARTICLE
    Birrell MA, Belvisi MG, Grace M, Sadofsky L, Faruqi S, Hele DJ, Maher SA, Freund-Michel V, Morice AHet al., 2009,

    TRPA1 Agonists Evoke Coughing in Guinea Pig and Human Volunteers

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 180, Pages: 1042-1047, ISSN: 1073-449X

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