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  • Conference paper
    Sheng TF, Huang H-Y, Chen J-K, Chung KF, Wang C-Het al., 2024,

    A newly-developed negative pressure ventilation (NPV) applied to patients with chronic obstructive pulmonary disease (COPD)

    , European-Respiratory-Society Congress (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
  • Conference paper
    Tran HM, Chuang H-C, Manullang A, Ho S-C, Lee K-Y, Chen K-Y, Chen T-T, Tseng C-H, Chung KFet al., 2024,

    Increased Risk of Severity in CCPD with Eosinophilic Inflammation due to Air Pollution Exposure

    , European-Respiratory-Society Congress (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
  • Conference paper
    Waziri H, Edwards DA, Bhatta DB, Hull J, Rudd M, Small P, Chung KFet al., 2024,

    Inhaled alkaline hypertonic divalent salts reduce refractory chronic cough frequency

    , Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
  • Conference paper
    Guo Y, Fenwick P, Viola P, Al-Sahaf M, Barnes PJ, Donnelly LEet al., 2024,

    Navitoclax inhibits senescence in human alveolar type 2 cells from COPD patients

    , European-Respiratory-Society Congress (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
  • Conference paper
    Valencia-Hernandez C, Wong E, Bloom C, 2024,

    Influence of pregnancy on asthma exacerbation patterns: a UK population-based cohort

    , European-Respiratory-Society Congress (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
  • Journal article
    Rupani H, Edwards D, Chaudhuri R, Smith S, Jackson DJ, Hearn A, Richards J, Moyses H, Kurukulaaratchy RJ, Haitchi HM, Edwards MR, Johnston SL, Djukanovic Ret al., 2024,

    Preserved antibody responses to COVID-19 vaccination and lower odds of developing COVID-19 in adults with severe asthma

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE, Vol: 12, ISSN: 2213-2198
  • Journal article
    Versi A, Azim A, Ivan FX, Abdel-Aziz M, Bates S, Riley J, Maitland-Van der Zee A, Dahlen S-E, Djukanovic R, Chotirmall S, Howarth P, Zounemat Kermani N, Chung KF, Adcock Iet al., 2024,

    Host-microbial interactions differ with age of asthma onset

    , European Respiratory Journal, Vol: 64, ISSN: 0903-1936
  • Journal article
    Versi A, Azim A, Ivan FX, Abdel-Aziz MI, Bates S, Riley J, Uddin M, Zounemat Kermani N, Maitland-Van Der Zee A-H, Dahlen S-E, Djukanovic R, Chotirmall SH, Howarth P, Adcock IM, Chung KF, UBIOPRED study groupet al., 2024,

    A severe asthma phenotype of excessive airway Haemophilus influenzae relative abundance associated with sputum neutrophilia

    , Clinical and Translational Medicine, Vol: 14, ISSN: 2001-1326

    BACKGROUND: Severe asthma (SA) encompasses several clinical phenotypes with a heterogeneous airway microbiome. We determined the phenotypes associated with a low α-diversity microbiome. METHODS: Metagenomic sequencing was performed on sputum samples from SA participants. A threshold of 2 standard deviations below the mean of α-diversity of mild-moderate asthma and healthy control subjects was used to define those with an abnormal abundance threshold as relative dominant species (RDS). FINDINGS: Fifty-one out of 97 SA samples were classified as RDSs with Haemophilus influenzae RDS being most common (n = 16), followed by Actinobacillus unclassified (n = 10), Veillonella unclassified (n = 9), Haemophilus aegyptius (n = 9), Streptococcus pseudopneumoniae (n = 7), Propionibacterium acnes (n = 5), Moraxella catarrhalis (n = 5) and Tropheryma whipplei (n = 5). Haemophilus influenzae RDS had the highest duration of disease, more exacerbations in previous year and greatest number on daily oral corticosteroids. Hierarchical clustering of RDSs revealed a C2 cluster (n = 9) of highest relative abundance of exclusively Haemophilus influenzae RDSs with longer duration of disease and higher sputum neutrophil counts associated with enrichment pathways of MAPK, NF-κB, TNF, mTOR and necroptosis, compared to the only other cluster, C1, which consisted of 7 Haemophilus influenzae RDSs out of 42. Sputum transcriptomics of C2 cluster compared to C1 RDSs revealed higher expression of neutrophil extracellular trap pathway (NETosis), IL6-transignalling signature and neutrophil activation. CONCLUSION: We describe a Haemophilus influenzae cluster of the highest relative abundance associated with neutrophilic inflammation and NETosis indicating a host response to the bacteria. This phenotype of severe asthma may respond to specific antibiotics.
  • Journal article
    Rhyou H-I, Kim H-K, Song W-J, Lee SM, Kim S-H, Kwon J-W, Park H-K, Park H-K, Kim SH, Choi J-H, Kim S, Park S-Y, Kim S-H, Moon J-Y, Jung J-W, Cho Y-J, Park CS, Kim BK, Kim J-H, Yang M-S, Kim M-H, Nam Y-H, Lee T, Lee B-J, Bhavsar P, Adcock IM, Chung KF, Kim T-Bet al., 2024,

    Effect of biologic therapies on quality of life in severe asthma: Findings from the PRISM study

    , The World Allergy Organization Journal, Vol: 17, ISSN: 1939-4551

    BACKGROUND: Anti-type 2 (T2) biologic therapies (biologics) improve exacerbation rates, lung function, and asthma-related quality of life (QoL) in patients with severe T2 asthma. However, studies comparing different biologics are lacking. We evaluated the QoL in patients with severe asthma comprehensively and compare the efficacy of different T2-directed biologics using QoL questionnaires. METHODS: We compared the QoL between severe and mild-to-moderate asthma and between severe asthma with and without biologics treatment. Data of mild-to-moderate were extracted from the Cohort for Reality and Evolution of Adult Asthma in Korea, and data of severe asthma were collected from the Precision Medicine Intervention in Severe Asthma. We included 183 patients with severe asthma treated with T2 biologics or conventional therapy between April 2020 and May 2021 and assessed QoL of them using the Questionnaire for Adult Korean Asthmatics (QLQAKA), Severe Asthma Questionnaire (SAQ), and EuroQoL-5Dimensions (EQ-5D) at baseline and 6 months. RESULTS: The EQ-5D index (0.803) of severe asthma was lower than that of other chronic diseases representing a worse QoL. The scores for all questions of QLQAKA, except "cough," were lower (less control) in the severe asthma group than in the mild-to-moderate asthma group at baseline and 6 months (P < 0.05). The total scores and subscores of all domains of the QLQAKA, SAQ, and EQ-5D improved significantly 6 months after biologic therapy but not after conventional therapy. The total QLQAKA, SAQ, and EQ-5D scores improved after 6 months in the anti-IL-5 (P < 0.05) and anti-IL-4/IL-13 (P < 0.05) treatment groups with no significant difference between groups (P > 0.05). CONCLUSION: QoL was worse in severe asthma than in mild-to-moderate asthma and other chronic diseases. T2 biologics equally improved QoL in patients with severe asthma.
  • Journal article
    Abdolmohammadi-Vahid S, Baradaran B, Adcock I, Mortaz Eet al., 2024,

    Immune checkpoint inhibitors and SARS-CoV2 infection

    , International Immunopharmacology, Vol: 137, ISSN: 1567-5769

    Infection with severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) triggers coronavirus disease 2019 (COVID-19), which predominantly targets the respiratory tract. SARS-CoV-2 infection, especially severe COVID-19, is associated with dysregulated immune responses against the virus, including exaggerated inflammatory responses known as the cytokine storm, together with lymphocyte and NK cell dysfunction known as immune cell exhaustion. Overexpression of negative immune checkpoints such as PD-1 and CTLA-4 plays a considerable role in the dysfunction of immune cells upon SARS-CoV-2 infection. Blockade of these checkpoints has been suggested to improve the clinical outcome of COVID-19 patients by promoting potent immune responses against the virus. In the current review, we provide an overview of the potential of checkpoint inhibitors to induce potent immune responses against SARS-CoV-2 and improving the clinical outcome of severe COVID-19 patients.
  • Journal article
    Thillai M, Oldham JM, Ruggiero A, Kanavati F, McLellan T, Saini G, Johnson SR, Ble F-X, Azim A, Ostridge K, Platt A, Belvisi M, Maher TM, Molyneaux PLet al., 2024,

    Deep Learning-based Segmentation of Computed Tomography Scans Predicts Disease Progression and Mortality in Idiopathic Pulmonary Fibrosis

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 210, Pages: 465-472, ISSN: 1073-449X
  • Journal article
    Hopkinson NS, 2024,

    The challenge of structural violence

    , BMJ: British Medical Journal, Vol: 386, ISSN: 0959-535X
  • Journal article
    Darquenne C, Corcoran TE, Lavorini F, Sorano A, Usmani OSet al., 2024,

    The effects of airway disease on the deposition of inhaled drugs

    , EXPERT OPINION ON DRUG DELIVERY, Vol: 21, Pages: 1175-1190, ISSN: 1742-5247
  • Journal article
    Bloom C, 2024,

    The burden of zoster in asthma: what is left to learn?

    , EUROPEAN RESPIRATORY JOURNAL, Vol: 64, ISSN: 0903-1936
  • Journal article
    Regis E, Fontanella S, Curtin JA, de Moira AP, Edwards MR, Murray CS, Simpson A, Johnston SL, Custovic Aet al., 2024,

    Association between polymorphisms on chromosome 17q12-q21 and rhinovirus-induced interferon responses

    , Journal of Allergy and Clinical Immunology, Vol: 154, Pages: 308-315, ISSN: 0091-6749

    Single nucleotide polymorphisms (SNPs) in genes on chromosome 17q12-q21 are associated with childhood-onset asthma and rhinovirus-induced wheeze. There are few mechanistic data linking chromosome 17q12-q21 to wheezing illness.ObjectiveWe investigated whether 17q12-q21 risk alleles were associated with impaired interferon responses to rhinovirus.MethodsIn a population-based birth cohort of European ancestry, we stimulated peripheral blood mononuclear cells with rhinovirus A1 (RV-A1) and rhinovirus A16 (RV-A16) and measured IFN and IFN-induced C-X-C motif chemokine ligand 10 (aka IP10) responses in supernatants. We investigated associations between virus-induced cytokines and 6 SNPs in 17q12-q21. Bayesian profile regression was applied to identify clusters of individuals with different immune response profiles and genetic variants.ResultsFive SNPs (in high linkage disequilibrium, r2 ≥ 0.8) were significantly associated with RV-A1–induced IFN-β (rs9303277, P = .010; rs11557467, P = .012; rs2290400, P = .006; rs7216389, P = .008; rs8079416, P = .005). A reduction in RV-A1–induced IFN-β was observed among individuals with asthma risk alleles. There were no significant associations for RV-A1–induced IFN-α or CXCL10, or for any RV-A16–induced IFN/CXCL10. Bayesian profile regression analysis identified 3 clusters that differed in IFN-β induction to RV-A1 (low, medium, high). The typical genetic profile of the cluster associated with low RV-A1–induced IFN-β responses was characterized by a very high probability of being homozygous for the asthma risk allele for all SNPs. Children with persistent wheeze were almost 3 times more likely to be in clusters with reduced/average RV-A1–induced IFN-β responses than in the high immune response cluster.ConclusionsPolymorphisms on chromosome 17q12-q21 are associated with rhinovirus-induced IFN-β, suggesting a novel mechanism—impaired IFN-β induction&md
  • Journal article
    Mortaz E, Roofchayee ND, Jamaati H, Varahram M, Abtahian Z, Mansourafshar B, Rekabi M, Adcock IM, Tabarsi Pet al., 2024,

    Long-standing COVID-19 Disease in Immunocompromised and Immunocompetent Patients; Case Reports and Literature Review

    , IRANIAN JOURNAL OF ALLERGY ASTHMA AND IMMUNOLOGY, Vol: 23, Pages: 457-466, ISSN: 1735-1502
  • Journal article
    Barnes PJ, 2024,

    Asthma-COPD coexistence

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 154, Pages: 275-277, ISSN: 0091-6749
  • Journal article
    Bousquet J, Sousa-Pinto B, Anto JM, Bedbrook A, Fonseca JA, Zuberbier T, MASK-air Think Tanket al., 2024,

    MASK-air: An OECD (Organisation for Economic Co-operation and Development) Best Practice for Public Health on Integrated Care for Chronic Diseases.

    , J Allergy Clin Immunol Pract, Vol: 12, Pages: 2010-2016.e7

    In the recent report of the Organisation for Economic Co-operation and Development (OECD) on Best Practices (BPs) for Integrating Care to Prevent and Manage Chronic Diseases, an app on rhinitis and asthma (MASK-air [Mobile Airways Sentinel networK for airway diseases]) has been listed. The OECD is a reliable source of evidence-based policy analysis and economic data largely used by governments. It has published several BPs on public health. On May 10, 2023, the OECD published 13 BPs for Integrating Care to Prevent and Manage Chronic Diseases in the European Union. The report did not cover all models of integrated care; rather, it "focuse(d) on those that are of key strategic interest to policy makers." New MASK-air studies (not published in the report) include equity, usability of the app in old-age adults, economic impact, quality of life, and allergen immunotherapy. MASK-air is freely available on iOS and Android in 30 countries and has been recently introduced in the United States. The MASK-air OECD BP represents a model of digitally enabled, patient-centered care for chronic diseases using a holistic approach of shared decision making.
  • Journal article
    Brasier AR, Zhao Y, Chung KF, 2024,

    Editorial: Mucosal adaptations to chronic airway injury: mechanisms and interrelationships of epithelial plasticity on innate immunity and airway remodeling

    , FRONTIERS IN IMMUNOLOGY, Vol: 15, ISSN: 1664-3224
  • Journal article
    Katsoulis O, Toussaint M, Jackson M, Mallia P, Footitt J, Mincham K, Meyer G, Kebadze T, Gilmour A, Long M, Aswani A, Snelgrove R, Johnston S, Chalmers J, Singanayagam Aet al., 2024,

    Neutrophil extracellular traps promote immunopathogenesis of virus-induced COPD exacerbations

    , Nature Communications, Vol: 15, ISSN: 2041-1723

    Respiratory viruses are a major trigger of exacerbations in chronic obstructive pulmonary disease (COPD). Airway neutrophilia is a hallmark feature of stable and exacerbated COPD but roles played by neutrophil extracellular traps (NETS) in driving disease pathogenesis are unclear. Here, using human studies of experimentally-induced and naturally-occurring exacerbations we identify that rhinovirus infection induces airway NET formation which is amplified in COPD and correlates with magnitude of inflammation and clinical exacerbation severity. We show that inhibiting NETosis protects mice from immunopathology in a model of virus-exacerbated COPD. NETs drive inflammation during exacerbations through release of double stranded DNA (dsDNA) and administration of DNAse in mice has similar protective effects. Thus, NETosis, through release of dsDNA, has a functional role in the pathogenesis of COPD exacerbations. These studies open up the potential for therapeutic targeting of NETs or dsDNA as a strategy for treating virus-exacerbated COPD.

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