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  • Conference paper
    Bloom CI, Sundaram V, Hubbard RB, Wedzicha JAet al., 2024,

    Association of Cardiovascular Disease, Pulmonary Embolism, and Pneumonia With Inhaled Corticosteroid Use in Asthma: A UK Cohort Study

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Fiorenzo E, Kumar K, Kebadze T, Mallia P, Singanayagam A, Edwards MR, Johnston SLet al., 2024,

    Clinically relevant β2-agonists induce and augment rhinovirus-induction of asthma- relevant pro-inflammatory mediators in human bronchial epithelial cells

    , International Conference of the American-Thoracic-Society (ATS), Publisher: American Thoracic Society, ISSN: 1073-449X
  • Conference paper
    Raby K, Koranteng JB, Dixey P, Adcock I, Gow ANM, Howarth P, Chung K, Bhavsar PKet al., 2024,

    Mepolizumab Depleted Blood Eosinophils Display a Reduced Adhesion Phenotype

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Kimura H, Kermani NZ, Adcock IM, Chung K, Kraft Met al., 2024,

    Association of CC16 Expression in the Airways With Signature Expression of Multi-omics Data

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Pyle CJ, Patel ND, Edwards MR, Shaw S, Johnston SLet al., 2024,

    A Rhinovirus VP0 Vaccine Induces Cross-reactive Type 1 Immunity and Promotes Lymphocyte Activation and Maturation

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Choy D, Nazarova E, Grimbaldeston M, Dugger D, Mar J, Chen H, Cheung DS, Johnston SL, Edwards MR, Morgan C, Park S, Trujillo-Torralbo M, Mallia P, Kon OM, Wilson M, Lafkas D, Chang Det al., 2024,

    A Stop-gain in FUT2 Associates With Several COPD Related Phenotypes and Clinical Outcomes

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Mar J, Dugger D, Chen H, Cheung DS, Morgan C, Park S, Trujillo-Torralbo M, Mallia P, Kon OM, Edwards MR, Johnston SL, Grimbaldeston M, Choy DFet al., 2024,

    Longitudinal Effects of Experimental Rhinovirus Challenge on Airway Phenotype in Chronic Obstructive Pulmonary Disease

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Bell J, Graul E, Nordon C, Kallis C, Whittaker HR, Janson C, Wilkinson AJK, Usmani OS, Quint JKet al., 2024,

    EXACOS CARBON: Describing the Greenhouse Gas Emissions of Healthcare Resource Utilization by Frequency and Severity of COPD Exacerbation in England

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Khalaf Z, Saglani S, Bloom CI, 2024,

    The Impact of Routine Asthma Reviews: A UK Population-based Cohort

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Journal article
    Cass SP, Nicolau DV, Baker JR, Mwasuku C, Ramakrishnan S, Mahdi M, Barnes PJ, Donnelly LE, Martinez-Nunez RT, Russell REK, Bafadhel Met al., 2024,

    Coordinated nasal mucosa-mediated immunity accelerates recovery from COVID-19

    , ERJ OPEN RESEARCH, Vol: 10
  • Conference paper
    Dixey P, Kermani NZ, Raby K, Bhavsar PK, Chung Ket al., 2024,

    Enose - Derived Response Clusters in Severe Asthmatics Treated With Anti-IL5/5R Biologics

    , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    MacKay J, Jucaite A, Cselenyi Z, Johnstrom P, Dahl K, Schou M, Stenkrona P, Sousa VC, Hognasbacka A, Gonzalez MAC, Giffen P, Bouma G, Nys J, Brulls M, Duncan M, Larsson J, Lundahl A, Les KA, Bergare J, Elmore CS, Kiraga J, Ble F-X, Fowler A, Belvisi MG, Marks DJet al., 2024,

    FIRST-TIME-IN-HUMAN VISUALISATION OF CCR9 EXPRESSION IN THE GUT BY POSITRON EMISSION TOMOGRAPHY

    , Digestive Disease Week (DDW), Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S605-S605, ISSN: 0016-5085
  • Journal article
    Jia M, Fu H, Jiang X, Wang L, Xu J, Barnes PJ, Adcock IM, Liu Y, He S, Zhang F, Yao L, Sun P, Yao Xet al., 2024,

    DEL-1, as an anti-neutrophil transepithelial migration molecule, inhibits airway neutrophilic inflammation in asthma

    , Allergy, Vol: 79, Pages: 1180-1194, ISSN: 0105-4538

    BackgroundNeutrophil migration into the airways is a key process in neutrophilic asthma. Developmental endothelial locus-1 (DEL-1), an extracellular matrix protein, is a neutrophil adhesion inhibitor that attenuates neutrophilic inflammation.MethodsLevels of DEL-1 were measured in exhaled breath condensate (EBC) and serum in asthma patients by ELISA. DEL-1 modulation of neutrophil adhesion and transepithelial migration was examined in a co-culture model in vitro. The effects of DEL-1-adenoviral vector-mediated overexpression on ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma were studied in mice in vivo.ResultsDEL-1 was primarily expressed in human bronchial epithelial cells and was decreased in asthma patients. Serum DEL-1 concentrations were reduced in patients with severe asthma compared with normal subjects (567.1 ± 75.3 vs. 276.8 ± 29.36 pg/mL, p < .001) and were negatively correlated to blood neutrophils (r = −0.2881, p = .0384) and neutrophil-to-lymphocyte ratio (NLR) (r = −0.5469, p < .0001). DEL-1 concentrations in the EBC of severe asthmatic patients (113.2 ± 8.09 pg/mL) were also lower than normal subjects (193.0 ± 7.61 pg/mL, p < .001) and were positively correlated with the asthma control test (ACT) score (r = 0.3678, p = .0035) and negatively related to EBC IL-17 (r = −0.3756, p = .0131), myeloperoxidase (MPO) (r = −0.5967, p = .0055), and neutrophil elastase (NE) (r = −0.5488, p = .0009) expression in asthma patients. Neutrophil adhesion and transepithelial migration in asthma patients were associated with LFA-1 binding to ICAM-1 and inhibited by DEL-1. DEL-1 mRNA and protein expression in human bro
  • Journal article
    Maneechotesuwan K, Prapruetkit N, Chankham J, Assawabhumi J, Kasetsinsombat K, Barnes PJet al., 2024,

    Paradoxical eosinophilic and cytokine responses to oral corticosteroid treatment in patients with asthma exacerbations

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: GLOBAL, Vol: 3
  • Journal article
    King GG, Chung LP, Usmani OS, Nilsen K, Thompson BRet al., 2024,

    Improving asthma outcomes: Clinicians' perspectives on peripheral airways

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY: GLOBAL, Vol: 3
  • Journal article
    Roth-Walter F, Adcock IM, Benito-Villalvilla C, Bianchini R, Bjermer L, Caramori G, Cari L, Chung KF, Diamant Z, Eguiluz-Gracia I, Knol EF, Jesenak M, Levi-Schaffer F, Nocentini G, O'Mahony L, Palomares O, Redegeld F, Sokolowska M, Van Esch BCAM, Stellato Cet al., 2024,

    Metabolic pathways in immune senescence and inflammaging: novel therapeutic strategy for chronic inflammatory lung diseases. An EAACI position paper from the Task Force for Immunopharmacology

    , Allergy, Vol: 79, Pages: 1089-1122, ISSN: 0105-4538

    The accumulation of senescent cells drives inflammaging and increases morbidity of chronic inflammatory lung diseases. Immune responses are built upon dynamic changes in cell metabolism that supply energy and substrates for cell proliferation, differentiation, and activation. Metabolic changes imposed by environmental stress and inflammation on immune cells and tissue microenvironment are thus chiefly involved in the pathophysiology of allergic and other immune-driven diseases. Altered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of proliferative activity in cells that remain metabolically active. Accelerated senescence can be triggered by acute or chronic stress and inflammatory responses. In contrast, replicative senescence occurs as part of the physiological aging process and has protective roles in cancer surveillance and wound healing. Importantly, cell senescence can also change or hamper response to diverse therapeutic treatments. Understanding the metabolic pathways of senescence in immune and structural cells is therefore critical to detect, prevent, or revert detrimental aspects of senescence-related immunopathology, by developing specific diagnostics and targeted therapies. In this paper, we review the main changes and metabolic alterations occurring in senescent immune cells (macrophages, B cells, T cells). Subsequently, we present the metabolic footprints described in translational studies in patients with chronic asthma and chronic obstructive pulmonary disease (COPD), and review the ongoing preclinical studies and clinical trials of therapeutic approaches aiming at targeting metabolic pathways to antagonize pathological senescence. Because this is a recently emerging field in allergy and clinical immunology, a better understanding of the metabolic profile of the complex landscape of cell senescence is needed. The progress achieved so far is already providing opportunities for new therapies, as well as for st
  • Journal article
    Suh DI, Johnston SL, 2024,

    The Wiser Strategy of Using Beta-Agonists in Asthma: Mechanisms and Rationales

    , ALLERGY ASTHMA & IMMUNOLOGY RESEARCH, Vol: 16, Pages: 217-234, ISSN: 2092-7355
  • Conference paper
    Harper AR, Bouma G, Lundahl A, Larsson J, Bock D, Eck S, Duncan M, Nys J, Mo J, Gehrmann U, Arkhammar P, Kiraga J, Popinska A, Soto PF, Belvisi MG, Fowler A, Marks DJet al., 2024,

    TOLERABILITY, SAFETY, AND CLINICAL PHARMACOLOGY OF AZD7798, A DEPLETING ANTIBODY TARGETING CCR9

    , Digestive Disease Week (DDW), Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S816-S817, ISSN: 0016-5085
  • Journal article
    Pinkerton JW, Preite S, Piras A, Zervas D, Markou T, Freeman MS, Hofving T, Ivarsson E, Bonvini SJ, Brailsford W, Yrlid L, Belvisi MG, Birrell MAet al., 2024,

    PI3Kγδ inhibition suppresses key disease features in a rat model of asthma

    , Respiratory Research, Vol: 25, ISSN: 1465-9921

    BACKGROUND: Two isoforms of Phosphoinositide 3-kinase (PI3K), p110γ and p110δ, are predominantly expressed in leukocytes and represent attractive therapeutic targets for the treatment of allergic asthma. The study aim was to assess the impact of administration of an inhaled PI3Kγδ inhibitor (AZD8154) in a rat model of asthma. METHODS: Firstly, we checked that the tool compound, AZD8154, inhibited rat PI3K γ & δ kinases using rat cell-based assays. Subsequently, a time-course study was conducted in a rat model of asthma to assess PI3K activity in the lung and how it is temporally associated with other key transcription pathways and asthma like features of the model. Finally, the impact on lung dosed AZD8154 on target engagement, pathway specificity, airway inflammation and lung function changes was assessed. RESULTS: Data showed that AZD8154 could inhibit rat PI3K γ & δ isoforms and, in a rat model of allergic asthma the PI3K pathway was activated in the lung. Intratracheal administration of AZD8154 caused a dose related suppression PI3K pathway activation (reduction in pAkt) and unlike after budesonide treatment, STAT and NF-κB pathways were not affected by AZD8154. The suppression of the PI3K pathway led to a marked inhibition of airway inflammation and reduction in changes in lung function. CONCLUSION: These data show that a dual PI3Kγδ inhibitor suppress key features of disease in a rat model of asthma to a similar degree as budesonide and indicate that dual PI3Kγδ inhibition may be an effective treatment for people suffering from allergic asthma.
  • Journal article
    Delfini Cancado JE, Usmani OS, 2024,

    Choice of inhaler device and its disposal have a significant impact on the environment

    , JORNAL BRASILEIRO DE PNEUMOLOGIA, Vol: 50, ISSN: 1806-3713

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