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• Journal article
  Deng R, Wang M, Chung KF, Zhu Yet al., 2025,

  Lung proteomic and metabolomic changes induced by carbon black nanoparticles and high humidity in a mouse asthma model

  , ENVIRONMENTAL POLLUTION, Vol: 367, ISSN: 0269-7491
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  • Citations: 1
• Journal article
  Heinemann L, Adcock I, Chung KF, Lollinga W, Hylkema MN, Papi A, Caramori G, Kirkham PAet al., 2025,

  Auto-antibodies against carbonyl-modified vimentin in COPD: potential role as a biomarker

  , JOURNAL OF INFLAMMATION-LONDON, Vol: 22, ISSN: 1476-9255
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• Journal article
  Xie Y, Li Y, Su Z, Han X, Liu Z, Huang Z, Cheng A, Zhou X, Li J, Qin R, Wei X, Liu Y, Xia X, Song Q, Zhao L, Chung KF, Xiao D, Wang Cet al., 2025,

  Estimating the association between cigarette and e-cigarette use patterns and SARS-CoV-2 negative conversion time: retrospective online survey in China

  , BMC INFECTIOUS DISEASES, Vol: 25
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• Journal article
  Tran HM, Tsai F-J, Wang Y-H, Lee K-Y, Chang J-H, Chung C-L, Tseng C-H, Su C-L, Lin Y-C, Chen T-T, Chen K-Y, Ho S-C, Yang F-M, Wu S-M, Chung KF, Ho K-F, Chuang K-J, Chuang H-Cet al., 2025,

  Joint effects of temperature and humidity with PM_2.5 on COPD

  , BMC PUBLIC HEALTH, Vol: 25
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  • Citations: 5
• Journal article
  Peltrini R, Cordell RL, Wilde M, Abuhelal S, Quek E, Zounemat-Kermani N, Ibrahim W, Richardson M, Brinkman P, Schleich F, Stefanuto PH, Aung H, Greening N, Dahlen SE, Djukanovic R, Adcock IM, Brightling C, Monks P, Siddiqui Set al., 2025,

  Discovery and Validation of a Volatile Signature of Eosinophilic Airway Inflammation in Asthma ( vol 210 , pg 1101 , 2024)

  , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 211, Pages: 296-296, ISSN: 1073-449X
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• Journal article
  Bloom CI, Yang F, Wedzicha JA, 2025,

  Reply to Chung et al. and to Rogliani and Calzetta

  , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 211, Pages: 293-294, ISSN: 1073-449X
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• Journal article
  Chung KF, Mazzone SB, Mcgarvey L, Song W-Jet al., 2025,

  Chronic cough as a disease: implications for practice, research, and health care

  , LANCET RESPIRATORY MEDICINE, Vol: 13, Pages: 110-112, ISSN: 2213-2600
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  • Citations: 4
• Journal article
  Sathyapala SA, Asimakopoulou K, Skinner TC, 2025,

  We must change our behaviour if CPAP adherence rates are to improve...

  , SLEEP MEDICINE, Vol: 126, Pages: 327-328, ISSN: 1389-9457
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• Conference paper
  Merchant Z, Naylor R, Malcolm R, Holmes H, Taylor M, Murray R, Callister ME, Hopkinson N, Agrawal S, Cheeseman H, Baldwin D, Goodley P, Alsaaty A, Balata H, Crosbie P, Booton R, Evison Met al., 2025,

  Evaluating the cost-effectiveness of integrated smoking cessation within lung cancer screening, using a health economic model

  , Publisher: ELSEVIER IRELAND LTD, Pages: 156-156, ISSN: 0169-5002
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• Journal article
  Gopalakrishnan V, Sparklin B, Kim JH, Bouquet J, Kehl M, Kenny T, Morehouse C, Caceres C, Warrener P, Hristova VA, Wilson S, Shandilya H, Barnes A, Ruzin A, Wang J, Oberg L, Angermann B, Mccrae C, Platt A, Muthas D, Hess S, Tkaczyk C, Sellman BR, Ostridge K, Belvisi MG, Wilkinson TMA, Staples KJ, Digiandomenico A, MICA II Study Grp Vet al., 2025,

  NTHi killing activity is reduced in COPD patients and is associated with a differential microbiome

  , RESPIRATORY RESEARCH, Vol: 26
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• Book chapter
  Barnes PJ, 2025,

  Oxidative stress in chronic obstructive pulmonary disease

  , Molecular Basis of Oxidative Stress Chemistry Toxicology Disease Pathogenesis Diagnosis and Therapeutics Second Edition, Pages: 381-393

  Oxidative stress is increasingly recognized as a major driving mechanism of chronic obstructive pulmonary disease (COPD) and an important target for future therapies. Oxidative stress in markedly increased in the lungs of COPD patients, as measured by increased breath concentrations of 8-isoprostane, ethane, and hydrogen peroxide. Exogenous oxidative stress from cigarette smoking and air pollution is a major risk factor for COPD and endogenous oxidative stress from reactive oxygen species released from activated inflammatory cells; particularly neutrophils and macrophages contribute to lung oxidative stress. Oxidative stress in COPD is further increased by reduced endogenous antioxidants and poor intake of dietary antioxidants. Oxidative stress is the major driving mechanism of COPD through induction of chronic inflammation, cellular senescence, impaired autophagy, reduced DNA repair, autoimmunity, increased mucus secretion, and impaired anti-inflammatory response to corticosteroids. Oxidative stress therefore drives the pathology of COPD, resulting in disease progression, amplification of exacerbations, and increased comorbidities through systemic oxidative stress. This suggests that antioxidants may be effective as disease-modifying treatments. Unfortunately, thiol-based antioxidants, such as N-acetylcysteine, have been poorly effective as they are inactivated by oxidative stress in the lungs, so there is a search for more effective and safe antioxidants, including mitochondria-targeted antioxidants, NOX inhibitors, and activators of the transcription factor Nrf2, which is impaired in COPD and regulates several antioxidant genes.

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• Conference paper
  Hedin CR, Creignou M, Mackay J, Jucaite A, Cselenyi Z, Johnstrom P, Dahl K, Schou M, Cortes Gonzalez MA, Hognasbacka A, Stenkrona P, Blomqvist LK, Cananau C, Palmer E, Bouma G, Eck S, Lund J, Lundahl A, Kiraga J, Popinska A, Eberhardson M, Belvisi MG, Marks DJBet al., 2025,

  Imaging of CCR9 in the small bowel of patients with Crohn's disease: effects of the CCR9-depleting monoclonal antibody AZD7798

  , Publisher: OXFORD UNIV PRESS, Pages: i2052-i2053, ISSN: 1873-9946
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• Conference paper
  Powell N, Hedin C, Harper AR, Mackay J, Lundin P, Bock D, Spata E, Bouma G, Tian S, Lundahl A, Lund J, Eck S, Popinska A, Strombeck A, Fowler A, Eberhardson M, Belvisi M, Marks DJBet al., 2025,

  AZD7798, a monoclonal antibody depleting CCR9+T cells, with the potential to target hard-to-treat small bowel Crohn's disease

  , Publisher: OXFORD UNIV PRESS, Pages: i1047-i1048, ISSN: 1873-9946
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• Journal article
  Devulder JV, Baker JR, Fenwick PS, Odqvist L, Donnelly LE, Barnes PJet al., 2025,

  COPD airway epithelial cell-derived extracellular vesicles spread cellular senescence via MicroRNA-34a

  , American Journal of Respiratory Cell and Molecular Biology, ISSN: 1044-1549

  Chronic obstructive pulmonary disease (COPD) is associated with the acceleration of lung aging, and the accumulation of senescent cells in lung tissue. MicroRNA (miR)-34a induces senescence by suppressing the anti-aging molecule, sirtuin-1 (SIRT1). Senescent cells spread senescence to neighbouring and distant cells, favouring COPD progression and its comorbidities. Mechanisms for spreading senescence remain undetermined but may be mediated by the transfer of microRNAs in extracellular vesicles. We analysed the miRNA content of extracellular vesicles in COPD and explored their effect on cellular senescence of healthy cells. EVs were isolated from small airway epithelial cells (SAEC) from healthy donors or COPD patients. Recipient healthy SAEC were cultured with EVs and the expression of miR-34a and markers of cellular senescence, p21CIP1 and SIRT1, were measured. We have shown that EVs from COPD cells induce senescence in healthy recipient cells via the selective transfer of miR-34a. COPD SAEC produce increased numbers of EVs enriched with miR-34a. EVs are taken up by healthy cells, resulting in reduced expression of the anti-aging molecule sirtuin-1 and increased expression of markers of senescence, like p21CIP1 and positive staining for senescence-associated β-galactosidase, which were blocked by a specific miR-34a antagomir. Our findings provide evidence of the mechanism by which EVs spread cellular senescence in human primary cells via miR-34a, rather than via soluble mediators. EVs enriched with miR-34a may spread senescence locally, accounting for disease progression, but also provide a mechanism for distant spread to account for comorbidities and multimorbidity of the elderly.

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• Journal article
  Baraldi F, Bartlett-Pestle S, Allinson JP, Macleod M, Mah J, Bloom C, Brady-Green A, Marion A, Papi A, Wedzicha JA, Finney LJet al., 2025,

  Blood eosinophil count stability in COPD and the eosinophilic exacerbator phenotype

  , American Journal of Respiratory and Critical Care Medicine, ISSN: 1073-449X
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• Journal article
  Kuks PJM, Kole TM, Kraft M, Siddiqui S, Fabbri LM, Rabe KF, Papi A, Brightling C, Singh D, van der Molen T, Kocks JWWH, Chung KF, Adcock IM, Bhavsar PK, Kermani NZ, Heijink IH, Pouwels SD, Kerstjens HAM, Slebos D-J, van den Berge Met al., 2025,

  Neutrophilic inflammation in sputum or blood does not define a clinically distinct asthma phenotype in ATLANTIS

  , ERJ Open Research, Vol: 11, Pages: 00616-2024, ISSN: 2312-0541

  IntroductionNeutrophilic asthma has been suggested to be a clinically distinct phenotype characterised by more severe airflow obstruction and higher exacerbation risk. However, this has only been assessed in few and smaller studies, using different cut-offs to define neutrophilia, and with conflicting results. We used data from ATLANTIS, an observational longitudinal study including a large number of patients with asthma and healthy controls. The aim of the present study was to examine whether neutrophilic inflammation, either in sputum or blood, is more prevalent in asthma and whether it correlates with disease severity.MethodsATLANTIS included 773 asthma patients, with blood collected from 767 (99%) and sputum from 228 patients (30%). Data were available from 244 healthy controls, all providing blood and 126 (52%) providing sputum. Asthma patients were characterised, including parameters of large and small airways disease at baseline and after 6 and 12 months of follow-up. Sputum and blood neutrophilia were defined as values exceeding the upper quartile in asthma patients.ResultsThe prevalence of sputum neutrophilia did not differ between asthma patients and healthy controls. Asthma patients with sputum neutrophilia did not display more severe symptoms, large or small airways disease or more frequent exacerbations. Blood neutrophilia was more common in asthma and was associated with higher body mass index, female sex, current smoking and systemic corticosteroid use. Patients with blood neutrophilia had a statistically significant, but small, increase in residual volume/total lung capacity. Blood neutrophilia was not associated with large or small airways disease or exacerbation risk.ConclusionSputum and blood neutrophilia do not define a distinct clinical phenotype in asthma.

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• Journal article
  Kang YR, Kim H, Lee CE, Jung J-W, Moon J-Y, Park SY, Kim S-H, Yang M-S, Kim BK, Kwon J-W, Park H-K, Nam Y-H, Cho Y-J, Lee T, Adcock IM, Bhavsar P, Chung KF, Kim T-Bet al., 2025,

  Serum and urine eosinophil-derived neurotoxin (EDN) levels predict biologic response in severe asthma

  , World Allergy Organization Journal, Vol: 18, ISSN: 1939-4551

  BackgroundEosinophils are crucial in allergic inflammation, and their correlation with asthma severity has made them a focal point in predicting treatment outcomes. Blood eosinophil count is a commonly utilized marker. However, its limitations have prompted alternative biomarker exploration, such as eosinophil-derived neurotoxin (EDN).ObjectiveThis research was conducted over 24 weeks on 56 patients with severe asthma treated with mepolizumab, reslizumab, and dupilumab. We aimed to evaluate the clinical significance of blood eosinophil count and their potential, including those of blood EDN levels and urine EDN values as biomarkers for predicting treatment response.MethodsThe analysis encompassed examining correlations between biomarkers and clinical features, including exacerbation rates and lung function, through ELISA assays and subsequent statistical analyses. The study protocol is registered at ClinicalTrials.gov (NCT05164939).ResultsThe findings underscore strong correlations between serum EDN levels, blood eosinophil counts, and treatment responses, with EDN demonstrating comparable predictive capabilities to blood eosinophil counts to determine treatment responses. Different biologics exhibited varying efficacy regarding baseline eosinophil counts and EDN levels.ConclusionsBlood eosinophil counts and EDN levels show potential as predictive markers for treatment responses in patients with severe asthma undergoing biologic therapies. However, further comprehensive studies are warranted to enhance the reliability and applicability of EDN as an effective asthma treatment biomarker.

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• Journal article
  Reddy KD, Xenaki D, Adcock IM, Oliver BGG, Zakarya Ret al., 2025,

  Epigenetic inhibitors differentially impact TGF-β1 signaling cascades in COPD airway smooth muscle cells

  , Cells, Vol: 14, Pages: 31-31, ISSN: 2073-4409

  Chronic obstructive pulmonary disease (COPD) is characterized by progressive and incurable airflow obstruction and chronic inflammation. Both TGF-β1 and CXCL8 have been well described as fundamental to COPD progression. DNA methylation and histone acetylation, which are well-understood epigenetic mechanisms regulating gene expression, are associated with COPD progression. However, a deeper understanding of the complex mechanisms associated with DNA methylation, histone post-translational changes and RNA methylation in the context of regulatory pathways remains to be elucidated. We here report on how DNA methylation and histone acetylation inhibition differentially affect CXCL8 signaling in primary human non-COPD and COPD airway cells. Methods: Airway smooth muscle (ASM) cells, a pivotal cell type in COPD, were isolated from the small airways of heavy smokers with and without COPD. Histone acetylation and DNA methylation were inhibited before the TGF-β1 stimulation of cells. Subsequently, CXCL8 production and the abundance and activation of pertinent transcription regulatory proteins (NF-κB, p38 MAPK and JNK) were analyzed. Results: TGF-β1-stimulated CXCL8 release from ASM cells from ‘healthy’ smoker subjects was significantly modulated by DNA methylation (56.32 pg/mL and 56.60 pg/mL) and acetylation inhibitors (27.50 pg/mL and 48.85 pg/mL) at 24 and 48 h, respectively. However, modulation via the inhibition of DNA methylation (34.06 pg/mL and 43.18 pg/mL) and acetylation (23.14 pg/mL and 27.18 pg/mL) was observed to a lesser extent in COPD ASM cells. These changes were associated with differences in the TGF-β1 activation of NF-κB and MAPK pathways at 10 and 20 min. Conclusions: Our findings offer insight into differential epigenetics in controlling COPD ASM cells and provide a foundation warranting future studies on epigenetic differences associated with COPD diagnosis. This would provide a scope for developing therapeutic

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• Journal article
  Tran HM, Tsai F-J, Lee K-Y, Wang Y-H, Yang F-M, Ho S-C, Bui HTM, Hoang LNN, Bui LTM, Ho K-F, Chung KF, Chuang K-J, Chuang H-Cet al., 2025,

  Extreme temperature increases the risk of COPD morbimortality: A systematic review and meta-analysis.

  , Sci Total Environ, Vol: 958

  INTRODUCTION: This systematic review examines how extreme temperatures impact chronic obstructive pulmonary disease (COPD) morbidity and mortality, focusing on identifying vulnerable subpopulations. METHODS: We conducted a systematic literature search from January 1, 2000, to November 6, 2024, across databases like PubMed, MEDLINE and EMBASE, Web of Science, and Scopus, focusing on observational studies that quantitatively defined extreme temperatures and their impacts on COPD morbidity and mortality. Out of 3140 records, 25 studies met the inclusion criteria. We extracted data on study characteristics, effect estimates, and confounders, employing methods to assess the risk of bias and synthesize results. RESULTS: We observed that extreme heat increased the relative risk (RR) for COPD morbimortality by 1.16-fold (95 % CI: 1.08-1.26; p < 0.05), and extreme cold increased the RR by 1.32-fold (95 % CI: 1.20-1.46;). Extreme heat was associated with a 1.19-fold (95 % CI: 1.09-1.30; p < 0.05) increase in COPD mortality. In contrast, extreme cold was associated with both COPD morbidity and mortality, with morbidity increasing by 1.47-fold (95 % CI: 1.26-1.71; p < 0.05) and mortality by 1.23-fold (95 % CI: 1.10-1.38; p < 0.05). Extreme heat poses a higher risk for female COPD patients compared to males. Moreover, extreme heat and cold were associated with morbimortality risk among older adults. Asian populations were sensitive to both temperature extremes, whereas Europeans were predominantly susceptible to extreme cold. CONCLUSION: This variability in response to extreme temperatures affects COPD morbidity and mortality, emphasizing the need for tailored medical and emergency responses to effectively mitigate health risks during extreme weather events.

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• Journal article
  Fiorenzo E, Senior P, Farne H, Siddiqui S, Singanayagam A, Johnston SLet al., 2025,

  Mechanisms of asthma exacerbations

  , Ers Monograph, Vol: 2025, Pages: 67-84, ISSN: 2312-508X

  Asthma exacerbations are an important public health issue with high morbidity and mortality. Most are caused by respiratory viral infections (largely rhinoviruses), although allergens and bacteria can also trigger exacerbations, both independently and in concert with viruses. Many people with asthma have deficient antiviral immunity, in part as a result of excess of IgE, eosinophils and the type 2 cytokines IL-4, IL-5 and IL-13. This leads to failure to control early viral replication, increased virus loads, and consequently, virus-load-driven increased type 2 and pro-inflammatory immune responses, as well as excess mucus production/secretion. β<inf>2</inf>-agonist overuse without ICS use is a risk factor for exacerbations, likely because ICS protect against the adverse effects of β<inf>2</inf>-agonists in addition to their anti-inflammatory prophylactic properties. There are multiple existing and potential therapeutic agents to prevent or treat exacerbations, including antiviral, anti-bacterial and immunomodulatory therapies. Further research is needed to better prevent and treat exacerbations.

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