Publications
411 results found
Belvisi MG, Dubuis E, Birrell MA, 2011, Transient Receptor Potential A1 Channels Insights Into Cough and Airway Inflammatory Disease, CHEST, Vol: 140, Pages: 1040-1047, ISSN: 0012-3692
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- Citations: 54
Eltom S, Stevenson CS, Rastrick J, et al., 2011, P2X7 receptor and caspase 1 activation are central to airway inflammation observed after exposure to tobacco smoke, PLoS ONE, Vol: 6, ISSN: 1932-6203
Chronic Obstructive Pulmonary Disease (COPD) is a cigarette smoke (CS)-driven inflammatory airway disease with anincreasing global prevalence. Currently there is no effective medication to stop the relentless progression of this disease. Ithas recently been shown that an activator of the P2X7/inflammasome pathway, ATP, and the resultant products (IL-1b/IL18) are increased in COPD patients. The aim of this study was to determine whether activation of the P2X7/caspase 1pathway has a functional role in CS-induced airway inflammation. Mice were exposed to CS twice a day to induce COPD-likeinflammation and the role of the P2X7 receptor was investigated. We have demonstrated that CS-induced neutrophilia in apre-clinical model is temporally associated with markers of inflammasome activation, (increased caspase 1 activity andrelease of IL-1b/IL-18) in the lungs. A selective P2X7 receptor antagonist and mice genetically modified so that the P2X7receptors were non-functional attenuated caspase 1 activation, IL-1b release and airway neutrophilia. Furthermore, wedemonstrated that the role of this pathway was not restricted to early stages of disease development by showing increasedcaspase 1 activation in lungs from a more chronic exposure to CS and from patients with COPD. This translational datasuggests the P2X7/Inflammasome pathway plays an ongoing role in disease pathogenesis. These results advocate thecritical role of the P2X7/caspase 1 axis in CS-induced inflammation, highlighting this as a possible therapeutic target incombating COPD.
Belvisi MG, Dale N, Birrell MA, et al., 2011, Bronchodilator activity of bitter tastants in human tissue, NATURE MEDICINE, Vol: 17, Pages: 776-776, ISSN: 1078-8956
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- Citations: 44
Maher SA, Dubuis ED, Belvisi MG, 2011, G-protein coupled receptors regulating cough, CURRENT OPINION IN PHARMACOLOGY, Vol: 11, Pages: 248-253, ISSN: 1471-4892
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- Citations: 34
Grace MS, Belvisi MG, 2011, TRPA1 receptors in cough, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 24, Pages: 286-288, ISSN: 1094-5539
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- Citations: 44
Schmidt LM, Belvisi MG, Bode KA, et al., 2011, Bronchial Epithelial Cell-Derived Prostaglandin E<sub>2</sub> Dampens the Reactivity of Dendritic Cells, JOURNAL OF IMMUNOLOGY, Vol: 186, Pages: 2095-2105, ISSN: 0022-1767
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- Citations: 44
Sadofsky LR, Boa AN, Maher SA, et al., 2011, TRPA1 is activated by direct addition of cysteine residues to the <i>N</i>-hydroxysuccinyl esters of acrylic and cinnamic acids, PHARMACOLOGICAL RESEARCH, Vol: 63, Pages: 30-36, ISSN: 1043-6618
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- Citations: 29
Rastrick JM, Eltom SM, Catley MC, et al., 2011, The In Vivo Characterisation Of An Acute And Sub-Chronic Model Of Cigarette Smoke-Induced Lung Inflammation, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Raemdonck K, Birrell MA, Belvisi MG, 2011, The Allergen Driven Late Asthmatic Response In Mice: A Role For Sensory Nerves And TRPA1, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Buckley J, Birrell MA, Maher SA, et al., 2011, EP4 Receptor Agonists: The Most Promising Novel Bronchodilator For Several Decades, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Maher SA, Clarke DL, Belvisi MG, 2011, Prostanoids, INFLAMMATION AND ALLERGY DRUG DESIGN, Editors: Izuhara, Holgate, WillsKarp, Publisher: BLACKWELL SCIENCE PUBL, Pages: 273-283, ISBN: 978-1-4443-3014-4
Slater L, Bartlett NW, Haas JJ, et al., 2010, Co-ordinated Role of TLR3, RIG-I and MDA5 in the Innate Response to Rhinovirus in Bronchial Epithelium, PLOS PATHOGENS, Vol: 6, ISSN: 1553-7366
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- Citations: 238
Birrell MA, Van Oosterhout AJM, Belvisi MG, 2010, Do the current house dust mite-driven models really mimic allergic asthma?, EUROPEAN RESPIRATORY JOURNAL, Vol: 36, Pages: 1220-1221, ISSN: 0903-1936
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- Citations: 16
Clarke DL, Clifford RL, Jindarat S, et al., 2010, TNFα and IFNγ Synergistically Enhance Transcriptional Activation of <i>CXCL10</i> in Human Airway Smooth Muscle Cells via STAT-1, NF-κB, and the Transcriptional Coactivator CREB-binding Protein, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 285, Pages: 29101-29110
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- Citations: 111
Freund-Michel VC, Birrell MA, Belvisi MG, 2010, Do β<sub>2</sub>-agonists inhibit capsaicin-induced cough?, EUROPEAN RESPIRATORY JOURNAL, Vol: 36, Pages: 460-461, ISSN: 0903-1936
Clarke DL, Clifford RL, Jindarat S, et al., 2010, TNF{alpha} and IFN{gamma} synergistically enhance transcriptional activation of CXCL10 in human airway smooth muscle cells via STAT-1, NF-{kappa}B and the transcriptional coactivator CREB-binding protein., J Biol Chem
Asthmatic airway smooth muscle (ASM) express interferon-gamma-inducible protein-10 (CXCL10), a chemokine known to mediate mast cell migration into ASM bundles that has been reported in the airways of asthmatic patients. CXCL10 is elevated in patients suffering from viral exacerbations of asthma and in patients with chronic obstructive pulmonary disease (COPD), diseases in which corticosteroids are largely ineffective. IFNgamma and TNFalpha synergistically induce CXCL10 release from HASM cells in a steroid-insensitive manner, via an as yet undefined mechanism. We report that TNFalpha activates the classical NF-kappaB pathway whereas IFNgamma activates JAK2/STAT-1alpha and that inhibition of the JAK/STAT pathway is more effective in abrogating CXCL10 release than the steroid fluticasone. The synergy observed with TNFalpha and IFNgamma together, however, did not lie at the level of NF-kappaB activation, STAT-1alpha phosphorylation or in vivo binding of these transcription factors to the CXCL10 promoter. Stimulation of HASM cells with TNFalpha and IFNgamma induced histone H4 but not histone H3 acetylation at the CXCL10 promoter, although no synergism was observed when both cytokines were combined. We show, however, that TNFalpha and IFNgamma exert a synergistic effect on the recruitment of CREB-binding Protein (CBP) to the CXCL10 which is accompanied by increased RNA polymerase II. Our results provide evidence that synergism between TNFalpha and IFNgamma lies at the level of coactivator recruitment in human ASM and suggest that inhibition of JAK/STAT signalling may be of therapeutic benefit in steroid-resistant airway disease.
De Alba J, Raemdonck K, Dekkak A, et al., 2010, House dust mite induces direct airway inflammation <i>in vivo</i>: implications for future disease therapy?, EUROPEAN RESPIRATORY JOURNAL, Vol: 35, Pages: 1377-1387, ISSN: 0903-1936
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- Citations: 38
Freund-Michel VC, Birrell MA, Giembycz MA, et al., 2010, β<sub>2</sub>-Agonists block tussive responses in guinea pigs <i>via</i> an atypical cAMP-dependent pathway, EUROPEAN RESPIRATORY JOURNAL, Vol: 35, Pages: 647-654, ISSN: 0903-1936
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- Citations: 25
Maher SA, Belvisi MG, 2010, Prostanoids and the Cough Reflex, LUNG, Vol: 188, Pages: S9-S12, ISSN: 0341-2040
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- Citations: 18
Bartlett NW, Walton RP, Caramori G, et al., 2010, Rhinovirus induces production of Th2 cell recruiting chemokines in vivo: linking infection and asthma exacerbations, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Eltom S, Raemdonck K, De Alba J, et al., 2010, House Dust Mite Exposure Induces Direct Non-Allergic Inflammation In Rodent Airways: Role Of The Innate Immune System, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 181, ISSN: 1073-449X
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- Citations: 1
Raemdonck K, De Alba J, Birrell MA, et al., 2010, A Role For Airway Sensory Nerves In The Allergen Induced Late Asthmatic Response In A Rat Model Of Allergic Asthma, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
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- Citations: 1
Maher SA, Grace MS, Birrell MA, et al., 2010, Prostaglandin E<sub>2</sub>-Induced Sensory Nerve Activation Is Mediated By TRPA1 And TRPV1, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
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- Citations: 3
Wong S, Birrell MA, Belvisi MG, et al., 2010, The role of MMP-9 and MMP-12 inhibitors in inflammation, NEW DRUGS AND TARGETS FOR ASTHMA AND COPD, Editors: Hansel, Publisher: KARGER, Pages: 231-235, ISBN: 978-3-8055-9566-7
Birrell MA, Belvisi MG, Grace M, et 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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- Citations: 213
Nasra J, Belvisi MG, 2009, Modulation of sensory nerve function and the cough reflex: Understanding disease pathogenesis, PHARMACOLOGY & THERAPEUTICS, Vol: 124, Pages: 354-375, ISSN: 0163-7258
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- Citations: 46
Maher SA, Birrell MA, Belvisi MG, 2009, Prostaglandin E<sub>2</sub> Mediates Cough via the EP<sub>3</sub> Receptor Implications for Future Disease Therapy, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 180, Pages: 923-928, ISSN: 1073-449X
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- Citations: 95
Belvisi MG, Mitchell JA, 2009, Targeting PPAR receptors in the airway for the treatment of inflammatory lung disease, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 158, Pages: 994-1003, ISSN: 0007-1188
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- Citations: 90
Wong S, Belvisi MG, Birrell MA, 2009, MMP/TIMP expression profiles in distinct lung disease models: implications for possible future therapies, Respiratory Research, Vol: 10, ISSN: 1465-9921
BackgroundThere is currently a vast amount of evidence in the literature suggesting that matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are involved in the pathogenesis of inflammatory airways diseases, such as asthma and COPD. Despite this, the majority of reports only focus on single MMPs, often only in one model system. This study aimed to investigate the profile of an extensive range of MMP/TIMP levels in three different pre-clinical models of airways disease. These models each have a different and very distinct inflammatory profile, each exhibiting inflammatory characteristics that are similar to that observed in asthma or COPD. Since these models have their own characteristic pathophysiological phenotype, one would speculate that the MMP/TIMP expression profile would also be different.MethodsWith the use of designed and purchased MMP/TIMP assays, investigation of rat MMP-2, 3, 7|14 and TIMP-1|4 mRNA expression was undertaken by Real Time PCR. The three rodent models of airways disease investigated were the endotoxin model, elastase model, and the antigen model.ResultsIntriguingly, we demonstrated that despite the distinct inflammatory profile observed by each model, the MMP/TIMP expression profile is similar between the models, in that the same MMPs/TIMPs were observed to be generally increased or decreased in all three models. It could therefore be speculated that in a particular disease, it may be a complex network of MMPs, rather than an individual MMP, together with inflammatory cytokines and other mediators, that results in the distinct phenotype of inflammatory diseases, such as asthma and COPD.ConclusionWe believe our data may provide key information necessary to understand the role of various MMPs/TIMPs in different inflammatory airway diseases, and aid the development of more selective therapeutics without the side effect profile of current broad-spectrum MMP inhibitors.
Edwards MR, Bartlett NW, Clarke D, et al., 2009, Targeting the NF-κB pathway in asthma and chronic obstructive pulmonary disease, PHARMACOLOGY & THERAPEUTICS, Vol: 121, Pages: 1-13, ISSN: 0163-7258
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- Citations: 305
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