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  • Journal article
    Lee CT, Ghandi SA, Elmrayed S, Barnes H, Lorenzetti D, Salibury ML, Stewart ID, Barber C, Peters CE, Feary J, Johannson KAet al., 2025,

    Inhalational exposures associated with risk of interstitial lung disease: a systematic review and meta-analysis

    , Thorax, Vol: 80, Pages: 918-926, ISSN: 0040-6376

    Rationale: Inhalational exposures are associated with risk of developing interstitial lung disease (ILD), yet the relationship between specific exposures and ILD is poorly characterized. Objective: Identify inhalational exposures associated with ILD and estimate the effects of exposures on ILD risk.Methods: MEDLINE and EMBASE databases were searched from 1990 until 2022 to identify inhalational exposures associated with ILD diagnosis. ILDs where causality is well-established (hypersensitivity pneumonitis, pneumoconiosis) and sarcoidosis were excluded. Two independent reviewers screened abstracts with full-text review and data extraction of eligible studies. Where possible, data were pooled and multi-level meta-analysis was specified using a random effects model. Sources of heterogeneity and risk of bias were assessed. Main Results: Ninety-six studies were included in the systematic review, representing 40,819,116 subjects (295,167 had ILD, 40,523,949 controls). For the meta-analysis, fifty-four studies were included (40,490,793 subjects: 273,899 ILD, 40,216,894 controls). Exposures associated with significantly increased ILD risk included smoking (OR 1.69, 95% CI 1.47-1.94), organic exposures (OR 1.56, 95% CI 1.12-2.16), metals (OR 1.52, 95% CI 1.07-2.16), dust (OR 1.45, 95% CI 1.20-1.76), and asbestos (OR 1.53, 95% CI 1.08-2.15). Silica and fumes had positive associations with ILD that trended toward significance. Conclusions: This systematic review and multilevel meta-analysis is the first to comprehensively assess the effect of inhalational exposures on overall risk of ILD, with multiple putative exposures identified. Future work should investigate novel occupational exposures associated with ILD, characterize the gene-environment interaction, and develop preventative strategies.
  • Journal article
    Madden VJ, Mqadi L, Arendse G, Bedwell GJ, Msolo N, Lesosky M, Hutchinson MR, Peter JG, Schrepf A, Parker R, Edwards RR, Joska JAet al., 2025,

    Provoked cytokine response is not associated with distress or induced secondary hyperalgesia in people with suppressed HIV

    , PAIN, Vol: 166, Pages: e830-e843, ISSN: 0304-3959
  • Journal article
    Allwood BW, Auld SC, Beko B, Bisson GP, Borges de Almeida CP, Byrne A, Chow FC, Davis A, Defres S, Drage M, Evans D, Gai X, Günther G, Gupte AN, Hoddinott G, Huaman MA, Huddart S, Huynh J, Kalyatanda G, Khosa C, Kutadza T, Makanda G, Marais S, Meghji J, Navuluri N, Nkereuwem E, Rajaratnam A, Romanowski K, Schoeman I, Seddon JA, Sohn H, Thienemann F, Wademan DT, Walker NF, van der Zalm MM, Nightingale Ret al., 2025,

    Proceedings from the Third International Post-Tuberculosis Symposium: expanding the circle.

    , IJTLD Open, Vol: 2, Pages: 727-738

    In light of the recent growth in interest and knowledge of post-TB sequelae, there were high levels of engagement during the 3rd International Post-Tuberculosis Symposium held in Stellenbosch, South Africa. This multi-disciplinary symposium aimed to: 1) Advocate for greater global awareness of post-TB sequelae and empower TB-affected communities; 2) Advance knowledge by sharing current evidence and identifying key priorities; 3) Foster collaborations by strengthening research networks and developing concrete plans for research driven advocacy; and 4) Advance the field by establishing areas of consensus around diagnosis, care, and management. Guided by a 14-member Steering Committee, 9 academic working groups came together to develop key content for plenary sessions and facilitated workshops related to: Patient Engagement, Epidemiology and Modelling, Pathogenesis, Post-TB Lung Disease; Cardiovascular and Pulmonary Vascular Disease; Central Nervous System and Musculoskeletal Disease; Paediatrics Economic; Social and Psychological Sequelae; and Advocacy, Policy, and Stakeholder Engagement. Each group outlined progress within their respective fields and defined key priorities to focus discussion. The Symposium further catalysed coordinated action for the post-TB community of patients, advocates, clinicians, and researchers to define a clear path towards improving outcomes, reducing inequities, and ensuring TB survivors receive the care and support they deserve.
  • Journal article
    Mayer-Hamblett N, Kerper NR, Clancy JP, Davies JC, Taylor-Cousar JL, Donaldson SH, Bell SC, Jain R, Simmonds NJ, Mall MA, Goss CH, Rayment JH, Setiawan L, Pilewski JMet al., 2025,

    Maximising opportunity for therapeutic success: sequential participation in cystic fibrosis nucleic acid-based therapy trials

    , LANCET RESPIRATORY MEDICINE, Vol: 13, ISSN: 2213-2600
  • Journal article
    Cabug AF, Crawford JC, Mcquilten HA, Foo IJH, Allen LF, Gebregzabher D, Mettelman RC, Novak T, Chou J, Rowntree LC, Hagen RR, Thomson AJ, Martin GE, Gilbertson B, Souter MN, James F, Goodall E, Rizzetto S, Flerlage T, Jia X, Van de Velde L-A, Chang SY, Luciani F, Thwaites RS, Trubiano JA, Kotsimbos TC, Cheng AC, Randolph AG, Thomas PG, Xu J, Wang Z, Nguyen THO, Chua BY, Kedzierski L, Kedzierska Ket al., 2025,

    High expression of interleukin-18 receptor alpha correlates with severe respiratory viral disease and defines T cells with reduced cytotoxic signatures

    , NATURE COMMUNICATIONS, Vol: 16
  • Journal article
    Sanchez-Burgos I, Tejedor AR, Collepardo-Guevara R, de la Serna JB, Espinosa JRet al., 2025,

    Molecular insights on the mechanism of α1-antitrypsin condensate formation and maturation

    , PLoS Computational Biology, Vol: 21, ISSN: 1553-734X

    The deficiency of -antitrypsin protein is a genetic disorder characterized by the accumulation of misfolded protein aggregates within hepatocytes, leading to liver dysfunction. In the lung, it is found in macrophages, bronchial and epithelial alveolar cells type 2, leading to pulmonary emphysema. Despite extensive research, the precise mechanism underlying the formation of -antitrypsin inclusion bodies remain elusive. In this study, we combine equilibrium and non-equilibrium molecular dynamics simulations to elucidate the intricate process of -antitrypsin condensate formation and maturation. Our mechanistic model explains cluster accumulation—specifically the onset of this pathogenesis—through the emergence of phase-separated liquid-like protein droplets, which subsequently undergo inter-protein β-sheet transitions between misfolded variants, resulting in solid-like clusters. We find that this mechanism only applies to the misfolded variant, Z--antitrypsin, which phase-separates driven by its disordered C-terminus. In contrast, the native protein, M--antitrypsin, shows much lower propensity to phase-separate and later form kinetically trapped aggregates. Furthermore, we explore how Z--antitrypsin exhibits an increased capacity to form condensates near external walls with different types of interactions. Such conditions can be similar to those found within the endoplasmic reticulum membrane, where phase separation and hardening take place. Overall, our results shed light on the molecular basis of -antitrypsin-related disorders and provide valuable microscopic insights for the development of therapeutic strategies targeting protein misfolding and aggregation-related disorders.
  • Journal article
    Green CG, Bempong J, Ong MLY, Shah A, Mallia P, Johnston SL, Singanayagam A, Reynolds JC, Heaney LMet al., 2025,

    Evaluating short-chain fatty acids in breath condensate as surrogate measurements for systemic levels and investigation into alternative respiratory sample matrices

    , Clinical Science, Vol: 139, Pages: 1287-1300, ISSN: 0143-5221

    Short-chain fatty acids (SCFAs) are metabolic by-products from microbial fermentation of complex carbohydrates and protein. They have gained clinical interest for their protective effects, including within the lung microenvironment. SCFAs are detectable in circulation and exhaled breath condensate (EBC), posing questions as to whether exhaled SCFAs originate from the gut and/or lung microbiota. Mapping SCFAs from the lung could improve our understanding of microbial activity in respiratory conditions. SCFA measurements in EBC were evaluated using a validated gas chromatography-mass spectrometry assay. Six healthy participants ingested sodium acetate, calcium propionate and sodium butyrate to acutely increase circulating SCFAs. EBC samples were collected alongside venous draws, with circulating and exhaled levels compared. A series of additional respiratory sample matrices from patient samples was investigated to gain novel insights into SCFAs within different respiratory biofluids. Serum SCFAs were increased in line with known responses. However, these increases were not observed in EBC, indicating a lack of correlation between circulating and exhaled SCFAs. SCFAs were detected in all additional respiratory biosamples, with EBC and sputum reporting the highest concentrations. Interestingly, branched-chain moieties were notably abundant in sputum, indicating the potential for their local production by bacterial fermentation of lung mucus proteins. SCFAs in EBC do not reflect circulatory levels and, therefore, are not a suitable surrogate measurement to inform on systemic load. These data suggest that exhaled SCFAs are potentially derived from lung microbial metabolism, supporting the need for further investigation into SCFA production, function and diagnostic utility in respiratory health.
  • Journal article
    Welham B, Bennett M, Ostridge K, Guy M, Zvavamwe C, Chilcott A, Johns S, Sundram F, Spalluto CM, Shaw E, Harden S, Alzetani A, Lee P, Lawson M, Lackie P, Michopoulou S, Henley D, Kong A, Fazleen A, Cellura D, Mccrae C, Platt A, Belvisi MG, Staples KJ, Wilkinson Tet al., 2025,

    A novel SPECT-CT imaging platform for quantifying in vivo lung cytokine signals in COPD

    , ERJ OPEN RESEARCH, Vol: 11
  • Journal article
    Sanchez-Garcia MA, Sadiku P, Ortmann BM, Wit N, Negishi Y, Coelho P, Zhang A, Pednekar C, Howden AJM, Griffith DM, Seear R, Kindrick JD, Mengede J, Cooper G, Morrison T, Watts ER, Shimeld BT, Reyes L, Mirchandani AS, Arienti S, Xu X, Thomson A, Brenes AJ, Turton HA, Dowey R, Hull RC, Davidson-Smith H, McLaren A, Deans A, Choudhury G, Doverman K, Hope D, Vick O, Woodhead A, Petrie I, Green S, Rzechorzek NM, Turtle L, Openshaw PJM, Semple MG, Sproul D, Baillie JK, Thompson AAR, Mole DR, Von Kriegsheim A, Whyte MKB, Mhalanga MM, Nathan JA, Walmsley SRet al., 2025,

    Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity

    , Nature Immunology, Vol: 26, ISSN: 1529-2908

    The long-term impact of systemic hypoxia resulting from acute respiratory distress syndrome (ARDS) on the function of short-lived innate immune cells is unclear. We show that patients 3–6 months after recovering from ARDS have persistently impaired circulating neutrophil effector functions and an increased susceptibility to secondary infections. These defects are linked to a widespread loss of the activating histone mark H3K4me3 in genes that are crucial for neutrophil activities. By studying healthy volunteers exposed to altitude-induced hypoxemia, we demonstrate that oxygen deprivation alone causes this long-term neutrophil reprogramming. Mechanistically, mouse models of systemic hypoxia reveal that persistent loss of H3K4me3 originates in proNeu and preNeu progenitors within the bone marrow and is linked to N-terminal histone 3 clipping, which removes the lysine residue for methylation. Thus, we present new evidence that systemic hypoxia initiates a sustained maladaptive reprogramming of neutrophil immunity by triggering histone 3 clipping and H3K4me3 loss in neutrophil progenitors.
  • Conference paper
    Chi S, Zhao H, Weinman J, Ma D, Ito K, Cookson WO, Moffatt MF, Zhang Yet al., 2025,

    P248 ORMDL3 influences ferroptosis through HMOX1 in human bronchial epithelial cells

    , British Thoracic Society Winter Meeting 2025, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 26 to 28 November 2025, Programme and Abstracts, Publisher: BMJ Publishing Group Ltd and British Thoracic Society, Pages: A301.1-A301
  • Conference paper
    Zhang Y, Du H, Guo H, Daly L, Wong J, Wang M, Chang E, Ma D, Ito K, Cookson WO, Moffatt MFet al., 2025,

    P249 Knockout of ORMDL3 renders airway epithelial cell resistance to human rhinovirus infection

    , British Thoracic Society Winter Meeting 2025, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 26 to 28 November 2025, Programme and Abstracts, Publisher: BMJ Publishing Group Ltd and British Thoracic Society, Pages: A301.2-A301
  • Journal article
    Szentpetery S, Riva D, Blumenfeld YJ, Engelhardt JF, Luna-Paredes C, Milla C, Schneider-Futschik EK, Sheffield JS, Darrah R, Davies JC, Flume PA, Foil KE, Fortner CN, Guimbellot JS, Lyerly AD, Mayer-Hamblett N, Ren CL, Spano J, Tillman EM, Trimble A, Wilfond BS, Taylor-Cousar JLet al., 2025,

    PRenatal mOdulator treatment to PrEvent CF complicaTions (PROTECT) workshop report

    , JOURNAL OF CYSTIC FIBROSIS, Vol: 24, Pages: 1058-1066, ISSN: 1569-1993
  • Journal article
    Pramanik SK, Sreedharan S, Kandoth N, de la Serna JB, Das A, Thomas JAet al., 2025,

    Transition metal complexes as optical probes for super-resolution microscopy

    , NATURE REVIEWS CHEMISTRY, Vol: 9, Pages: 733-748
  • Conference paper
    Du H, Ma J, Lei M, Guo H, Daly L, Zhang E, Wang M, Ito K, Cookson WO, Moffatt MF, Zhang Yet al., 2025,

    P250 GSDMB regulates human rhinovirus replication and inflammation in airway epithelial cells

    , British Thoracic Society Winter Meeting 2025, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 26 to 28 November 2025, Programme and Abstracts, Publisher: BMJ Publishing Group Ltd and British Thoracic Society, Pages: A301.3-A302
  • Conference paper
    Zhang Y, Tanro M, Chi S, Chang E, Wang M, Ma Z, Zhao H, Ito K, Ma D, Cookson WO, Moffatt MFet al., 2025,

    P247 GSDMB mediates epithelial to mesenchymal transition (EMT) in human airway epithelial cells

    , British Thoracic Society Winter Meeting 2025, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 26 to 28 November 2025, Programme and Abstracts, Publisher: BMJ Publishing Group Ltd and British Thoracic Society, Pages: A300-A301
  • Journal article
    Wilson G, Hughes D, 2025,

    Aging gracefully: does elexacaftor/tzacaftor/ivacaftor safety and efficacy stand the test of time?

    , American Journal of Respiratory and Critical Care Medicine, Vol: 211, Pages: 1893-1895, ISSN: 1073-449X
  • Journal article
    Dobra R, Short C, Wong K, Saunders C, Abkir M, Irving S, Davies JCet al., 2025,

    Utility and interpretation of multiple breath washout in children with cystic fibrosis

    , Archives of Disease in Childhood: Education and Practice Edition, Vol: 110, Pages: 214-217, ISSN: 1743-0585

    Transformative changes in the health of children with cystic fibrosis (CF) mean that more sensitive outcome measures are needed to monitor paediatric CF lung disease. Multiple breath washout (MBW) and its primary readout lung clearance index are gaining increasing traction as an endpoint for clinical trials in the CF space and show promise as a clinical investigation. In this article, we use four clinically based questions to explore what MBW can and cannot (yet) do and highlight some of its strengths and weaknesses as an investigation. We end by discussing how we can increase the utility of MBW as an investigation in children with CF.
  • Journal article
    Wainwright C, McColley SA, McNally P, Powers M, Ratjen F, Rayment JH, Retsch-Bogart G, Roesch E, Ramsey B, Mckone EF, Tullis E, Mall MA, Taylor-Cousar JL, Waltz D, Ahluwalia N, Chu C, Scirica C, Davies JCet al., 2025,

    Long-Term Safety and Efficacy of Elexacaftor/Tezacaftor/Ivacaftor in Children ≥6 Years with Cystic Fibrosis and at Least One <i>F508del</i> Allele: A 192-Week, Phase 3, Open-Label Extension Study

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 211, Pages: 1915-1925, ISSN: 1073-449X
  • Journal article
    Rowland SN, Green CG, Halliwill JR, Singanayagam A, Heaney LMet al., 2025,

    Gut feelings on short-chain fatty acids to regulate respiratory health.

    , Trends Endocrinol Metab, Vol: 36, Pages: 889-898

    Respiratory infections and diseases pose significant challenges to society and healthcare systems, underscoring the need for preventative and therapeutic strategies. Recent research in rodent models indicates that short-chain fatty acids (SCFAs), metabolites produced by gut bacteria, may offer medicinal benefits for respiratory conditions. In this opinion, we summarize the current literature that highlights the potential of SCFAs to enhance immune balance in humans. SCFAs have demonstrated the potential to decrease the risk of primary and secondary respiratory infections, modulate allergic airway exacerbations, and improve overall epithelial pathogen defenses. Therefore, we suggest that systemic SCFA levels could be targeted to support gut and respiratory health in specific groups, such as patients in hospital, women and their offspring, children, older adults, and athletes/military personnel.
  • Journal article
    Tomeny EM, Tran PB, Kazibwe J, Rosu L, Nikolaidis GF, Nightingale R, Wingfield T, Meghji J, Squire SB, Worrall Eet al., 2025,

    A broader lens on tuberculosis cost-effectiveness analysis: How patient-incurred costs and post-tuberculosis outcomes reshape estimates in a multi-country study

    , PLOS GLOBAL PUBLIC HEALTH, Vol: 5

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