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  • Journal article
    Chang P-J, Michaeloudes C, Zhu J, Shaikh N, Baker J, Chung KF, Bhavsar PKet al., 2015,

    Impaired nuclear translocation of the glucocorticoid receptor in corticosteroid-insensitive airway smooth muscle in severe asthma

    , American Journal of Respiratory and Critical Care Medicine, Vol: 191, Pages: 54-62, ISSN: 1073-449X

    Rationale: Patients with severe asthma (SA) are less responsive to the beneficial effects of corticosteroid (CS) therapy, and relative CS insensitivity has been shown in airway smooth muscle cells (ASMC) from patients with SA.Objectives: We investigated whether there was a defect in the actions of the glucocorticoid receptor (GR) underlying the ability of CS to suppress the inflammatory response in ASMC of patients with SA. ASMC from healthy subjects (n = 10) and subjects with severe (n = 8) and nonsevere asthma (N-SA; n = 8) were cultured from endobronchial biopsies.Measurements and Main Results: GR expression in ASMC from SA and N-SA was reduced compared with that from healthy subjects by 49% (P < 0.01). Although baseline levels of nuclear GR were similar, GR nuclear translocation induced by dexamethasone (10−7 M) in SA was 60% of that measured in either healthy subjects or subjects with N-SA. Tumor necrosis factor (TNF)-α induced greater nuclear factor (NF)-κB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-α–induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups. Dexamethasone, although not modulating TNF-α–induced p65 nuclear translocation, attenuated p65 recruitment to the CCL11 promoter in the healthy and N-SA groups, but this suppressive effect was impaired in subjects with SA.Conclusions: Decreased GR expression with impaired nuclear translocation in ASMC, associated with reduced dexamethasone-mediated attenuation of p65 recruitment to NF-κB–dependent gene promoters, may underlie CS insensitivity of severe asthma.
  • Journal article
    Mortaz E, Adcock IM, Tabarsi P, Masjedi MR, Masjedi MR, Mansouri D, Velayati AA, Casanova J-L, Barnes PJet al., 2015,

    Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis.

    , Journal of clinical immunology, Vol: 35, Pages: 1-10, ISSN: 0271-9142

    Tuberculosis (TB) is considered a major worldwide health problem with 10 million new cases diagnosed each year. Our understanding of TB immunology has become greater and more refined since the identification of Mycobacterium tuberculosis (MTB) as an etiologic agent and the recognition of new signaling pathways modulating infection. Understanding the mechanisms through which the cells of the immune system recognize MTB can be an important step in designing novel therapeutic approaches, as well as improving the limited success of current vaccination strategies. A great challenge in chronic disease is to understand the complexities, mechanisms, and consequences of host interactions with pathogens. Innate immune responses along with the involvement of distinct inflammatory mediators and cells play an important role in the host defense against the MTB. Several classes of pattern recognition receptors (PRRs) are involved in the recognition of MTB including Toll-Like Receptors (TLRs), C-type lectin receptors (CLRs) and Nod-like receptors (NLRs) linked to inflammasome activation. Among the TLR family, TLR1, TLR2, TLR4, and TLR9 and their down-stream signaling proteins play critical roles in the initiation of the immune response in the pathogenesis of TB. The inflammasome pathway is associated with the coordinated release of cytokines such as IL-1β and IL-18 which also play a role in the pathogenesis of TB. Understanding the cross-talk between these signaling pathways will impact on the design of novel therapeutic strategies and in the development of vaccines and immunotherapy regimes. Abnormalities in PRR signaling pathways regulated by TB will affect disease pathogenesis and need to be elucidated. In this review we provide an update on PRR signaling during M. tuberculosis infection and indicate how greater knowledge of these pathways may lead to new therapeutic opportunities.
  • Journal article
    Liang Z, Zhang Q, Thomas CMR, Chana KK, Gibeon D, Barnes PJ, Chung KF, Bhavsar PK, Donnelly LEet al., 2014,

    Impaired macrophage phagocytosis of bacteria in severe asthma

    , RESPIRATORY RESEARCH, Vol: 15
  • Journal article
    Dubuis E, Wortley MA, Grace MS, Maher SA, Adcock JJ, Birrell MA, Belvisi MGet al., 2014,

    Theophylline inhibits the cough reflex through a novel mechanism of action

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 133, Pages: 1588-1598, ISSN: 0091-6749
  • Journal article
    Birrell MA, Bonvini SJ, Dubuis E, Maher SA, Wortley MA, Grace MS, Raemdonck K, Adcock JJ, Belvisi MGet al., 2014,

    Tiotropium modulates transient receptor potential V1 (TRPV1) in airway sensory nerves: A beneficial off-target effect?

    , Journal of Allergy and Clinical Immunology, Vol: 133, Pages: 679-687.e9, ISSN: 0091-6749

    BackgroundRecent studies have suggested that the long-acting muscarinic receptor antagonist tiotropium, a drug widely prescribed for its bronchodilator activity in patients with chronic obstructive pulmonary disease and asthma, improves symptoms and attenuates cough in preclinical and clinical tussive agent challenge studies. The mechanism by which tiotropium modifies tussive responses is not clear, but an inhibition of vagal tone and a consequent reduction in mucus production from submucosal glands and bronchodilation have been proposed.ObjectiveThe aim of this study was to investigate whether tiotropium can directly modulate airway sensory nerve activity and thereby the cough reflex.MethodsWe used a conscious cough model in guinea pigs, isolated vagal sensory nerve and isolated airway neuron tissue– and cell-based assays, and in vivo single-fiber recording electrophysiologic techniques.ResultsInhaled tiotropium blocked cough and single C-fiber firing in the guinea pig to the transient receptor potential (TRP) V1 agonist capsaicin, a clinically relevant tussive stimulant. Tiotropium and ipratropium, a structurally similar muscarinic antagonist, inhibited capsaicin responses in isolated guinea pig vagal tissue, but glycopyrrolate and atropine did not. Tiotropium failed to modulate other TRP channel–mediated responses. Complementary data were generated in airway-specific primary ganglion neurons, demonstrating that tiotropium inhibited capsaicin-induced, but not TRPA1-induced, calcium movement and voltage changes.ConclusionFor the first time, we have shown that tiotropium inhibits neuronal TRPV1-mediated effects through a mechanism unrelated to its anticholinergic activity. We speculate that some of the clinical benefit associated with taking tiotropium (eg, in symptom control) could be explained through this proposed mechanism of action.
  • Journal article
    Bernardino de la Serna J, Hansen S, Berzina Z, Simonsen AC, Hannibal-Bach HK, Knudsen J, Ejsing CS, Bagatolli LAet al., 2013,

    Compositional and structural characterization of monolayers and bilayers composed of native pulmonary surfactant from wild type mice

    , BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES, Vol: 1828, Pages: 2450-2459, ISSN: 0005-2736
  • Journal article
    Damby DE, Horwell CJ, Baxter PJ, Delmelle P, Donaldson K, Dunster C, Fubini B, Murphy FA, Nattrass C, Sweeney S, Tetley TD, Tomatis Met al., 2013,

    The respiratory health hazard of tephra from the 2010 Centennial eruption of Merapi with implications for occupational mining of deposits

    , JOURNAL OF VOLCANOLOGY AND GEOTHERMAL RESEARCH, Vol: 261, Pages: 376-387, ISSN: 0377-0273
  • Journal article
    Bernardino de la Serna J, Vargas R, Picardi V, Cruz A, Arranz R, Valpuesta JM, Mateu L, Perez-Gil Jet al., 2013,

    Segregated ordered lipid phases and protein-promoted membrane cohesivity are required for pulmonary surfactant films to stabilize and protect the respiratory surface

    , FARADAY DISCUSSIONS, Vol: 161, Pages: 535-548, ISSN: 1359-6640
  • Journal article
    O'Rourke J, Wang WP, Donnelly L, Wang E, Kreutzer DLet al., 1987,

    Extravascular plasminogen activator and inhibitor activities detected at the site of a chronic mycobacterial-induced inflammation

    , American Journal of Pathology, ISSN: 1525-2191

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