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Journal articleBunyavanich S, Becker PM, Altman MC, et al., 2024,
Analytical challenges in omics research on asthma and allergy: A National Institute of Allergy and Infectious Diseases workshop
, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 153, Pages: 954-968, ISSN: 0091-6749 -
Journal articleGancitano G, Mucci N, Stange R, et al., 2024,
Echinacea Reduces Antibiotics by Preventing Respiratory Infections: A Meta-Analysis (ERA-PRIMA)
, ANTIBIOTICS-BASEL, Vol: 13, ISSN: 2079-6382 -
Journal articleBurgess JK, Weiss DJ, Westergren-Thorsson G, et al., 2024,
Extracellular matrix as a driver of chronic lung diseases
, American Journal of Respiratory Cell and Molecular Biology, Vol: 70, Pages: 239-246, ISSN: 1044-1549The extracellular matrix (ECM) is not just a 3 dimensional scaffold that provides stable support for all cells in the lungs but is also an important component of chronic fibrotic airways, vascular, and interstitial diseases. It is a bioactive entity that is dynamically modulated during tissue homeostasis and disease, which controls structural and immune cell functions, drug responses, and which can release fragments that have biological activity and that can be used to monitor disease activity. There is a growing recognition of the importance of considering ECM changes in chronic airways, vascular, and interstitial diseases including (i) compositional changes, (ii) structural and organizational changes, and (iii) mechanical changes -and how these impact on disease pathogenesis. Since altered ECM biology is an important component of many lung diseases, disease models must incorporate this factor to fully recapitulate disease-driver pathways and to study potential novel therapeutic interventions. While novel models are evolving that capture some or all of the elements of the altered ECM microenvironment in lung diseases, opportunities exist to more fully understand cell-ECM interactions that will help devise future therapeutic targets to restore function in chronic lung diseases. In this perspective article, we review evolving knowledge about the ECM's role in homeostasis and disease in the lung.
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Journal articleOh J-Y, Kang S-Y, Kang N, et al., 2024,
Characterization of Codeine Treatment Responders Among Patients with Refractory or Unexplained Chronic Cough: A Prospective Real-World Cohort Study
, LUNG, Vol: 202, Pages: 97-106, ISSN: 0341-2040 -
Journal articleWrench CL, Baker JR, Monkley S, et al., 2024,
Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence
, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 326, Pages: L266-L279, ISSN: 1040-0605 -
Journal articleWeng J, Liu Q, Li C, et al., 2024,
TRPA1-PI3K/Akt-OPA1-ferroptosis axis in ozone-induced bronchial epithelial cell and lung injury
, Science of the Total Environment, Vol: 918, ISSN: 0048-9697BACKGROUND: Transient receptor potential (TRP) ankyrin 1 (TRPA1) could mediate ozone-induced lung injury. Optic Atrophy 1 (OPA1) is one of the significant mitochondrial fusion proteins. Impaired mitochondrial fusion, resulting in mitochondrial dysfunction and ferroptosis, may drive the onset and progression of lung injury. In this study, we examined whether TRPA1 mediated ozone-induced bronchial epithelial cell and lung injury by activating PI3K/Akt with the involvement of OPA1, leading to ferroptosis. METHODS: Wild-type, TRPA1-knockout (KO) mice (C57BL/6 J background) and ferrostatin-1 (Fer-1)-pretreated mice were exposed to 2.5 ppm ozone for 3 h. Human bronchial epithelial (BEAS-2B) cells were treated with 1 ppm ozone for 3 h in the presence of TRPA1 inhibitor A967079 or TRPA1-knockdown (KD) as well as pharmacological modulators of PI3K/Akt-OPA1-ferroptosis. Transcriptome was used to screen and decipher the differential gene expressions and pathways. Oxidative stress, inflammation and ferroptosis were measured together with mitochondrial morphology, function and dynamics. RESULTS: Acute ozone exposure induced airway inflammation and airway hyperresponsiveness (AHR), reduced mitochondrial fusion, and enhanced ferroptosis in mice. Similarly, acute ozone exposure induced inflammatory responses, altered redox responses, abnormal mitochondrial structure and function, reduced mitochondrial fusion and enhanced ferroptosis in BEAS-2B cells. There were increased mitochondrial fusion, reduced inflammatory responses, decreased redox responses and ferroptosis in ozone-exposed TRPA1-KO mice and Fer-1-pretreated ozone-exposed mice. A967079 and TRPA1-KD enhanced OPA1 and prevented ferroptosis through the PI3K/Akt pathway in BEAS-2B cells. These in vitro results were further confirmed in pharmacological modulator experiments. CONCLUSION: Exposure to ozone induces mitochondrial dysfunction in human bronchial epithelial cells and mouse lungs by activating T
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Journal articleGilworth G, Harris K, Morgan TL, et al., 2024,
The IMPROVE trial: study protocol for a pragmatic cluster randomised controlled trial to assess the effectiveness of using lay health workers to improve uptake and completion of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease
, Trials, Vol: 25, ISSN: 1745-6215BACKGROUND: Pulmonary rehabilitation (PR) is a programme of exercise and education and the most effective treatment for the symptoms and disability associated with chronic obstructive pulmonary disease. However, the benefits of PR are limited by poor uptake and completion. This trial will determine whether using trained volunteer lay health workers, called "PR buddies," improves uptake and completion of PR and is cost-effective. This trial protocol outlines the methods for evaluating effectiveness, cost-effectiveness, and acceptability. METHODS: The IMPROVE trial is a pragmatic, open, cluster randomised controlled trial planned in 38 PR services across England and Wales. PR services will be randomised to either intervention arm-offering support from PR buddies to patients with chronic obstructive pulmonary disease-or to usual care as the control arm. PR staff in trial sites randomised to the intervention arm will receive training in recruiting and training PR buddies. They will deliver training to volunteers, recruited from among people who have recently completed PR in their service. The 3-day PR-buddy training programme covers communication skills, confidentiality, boundaries of the PR-buddy role and behaviour change techniques to help patients overcome obstacles to attending PR. An internal pilot will test the implementation of the trial in eight sites (four intervention sites and four in control arm). The primary outcome of the trial is the uptake and completion of PR. A process evaluation will investigate the acceptability of the intervention to patients, PR staff and the volunteer PR buddies, and intervention fidelity. We will also conduct a cost-effectiveness analysis. DISCUSSION: Improving outcomes for chronic obstructive pulmonary disease and access to PR are priorities for the UK National Health Service (NHS) in its long-term plan. The trial hypothesis is that volunteer PR buddies, who are recruited and trained by local PR teams, are an effective
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Journal articleHopkinson NS, 2024,
Reply to Pacheco Gallego and Farber, to Young et al., and to Aslan.
, American Journal of Respiratory and Critical Care Medicine, Vol: 209, Pages: 761-762, ISSN: 1073-449X -
Journal articleMelén E, Faner R, Allinson JP, et al., 2024,
Lung-function trajectories: relevance and implementation in clinical practice
, The Lancet, ISSN: 0140-6736Lung development starts in utero and continues during childhood through to adolescence, reaching its peak in early adulthood. This growth is followed by gradual decline due to physiological lung ageing. Lung-function development can be altered by several host and environmental factors during the life course. As a result, a range of lung-function trajectories exist in the population. Below average trajectories are associated with respiratory, cardiovascular, metabolic, and mental health comorbidities, as well as with premature death. This Review presents progressive research into lung-function trajectories and assists the implementation of this knowledge in clinical practice as an innovative approach to detect poor lung health early, monitor respiratory disease progression, and promote lung health. Specifically, we propose that, similar to paediatric height and weight charts used globally to monitor children's growth, lung-function charts could be used for both children and adults to monitor lung health status across the life course. To achieve this proposal, we introduce our free online Lung Function Tracker tool. Finally, we discuss challenges and opportunities for effective implementation of the trajectory concept at population level and outline an agenda for crucial research needed to support such implementation.
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Journal articleDelgado-Ortiz L, Ranciati S, Arbillaga-Etxarri A, et al., 2024,
Real-world walking cadence in people with COPD
, ERJ Open Research, Vol: 10, ISSN: 2312-0541Introduction The clinical validity of real-world walking cadence in people with COPD is unsettled. Our objective was to assess the levels, variability and association with clinically relevant COPD characteristics and outcomes of real-world walking cadence.Methods We assessed walking cadence (steps per minute during walking bouts longer than 10 s) from 7 days’ accelerometer data in 593 individuals with COPD from five European countries, and clinical and functional characteristics from validated questionnaires and standardised tests. Severe exacerbations during a 12-month follow-up were recorded from patient reports and medical registries.Results Participants were mostly male (80%) and had mean±sd age of 68±8 years, post-bronchodilator forced expiratory volume in 1 s (FEV1) of 57±19% predicted and walked 6880±3926 steps·day−1. Mean walking cadence was 88±9 steps·min−1, followed a normal distribution and was highly stable within-person (intraclass correlation coefficient 0.92, 95% CI 0.90–0.93). After adjusting for age, sex, height and number of walking bouts in fractional polynomial or linear regressions, walking cadence was positively associated with FEV1, 6-min walk distance, physical activity (steps·day−1, time in moderate-to-vigorous physical activity, vector magnitude units, walking time, intensity during locomotion), physical activity experience and health-related quality of life and negatively associated with breathlessness and depression (all p<0.05). These associations remained after further adjustment for daily steps. In negative binomial regression adjusted for multiple confounders, walking cadence related to lower number of severe exacerbations during follow-up (incidence rate ratio 0.94 per step·min−1, 95% CI 0.91–0.99, p=0.009).Conclusions Higher real-world walking cadence is associated with better COPD status and lower severe exacerbations risk, w
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Journal articleKoranteng J, Chung KF, Michaeloudes C, et al., 2024,
The role of mitochondria in eosinophil function: implications for severe asthma pathogenesis
, FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, Vol: 12, ISSN: 2296-634X -
Book chapterDonnelly L, Devulder J, 2024,
Mechanisms and Mediatiors of Disease
, COPD in the 21st Century, Editors: Wedzicha, Allinson, Calverley, Publisher: ERS, Pages: 100-117COPD is a common respiratory condition characterised by airway limitation and changes in airway structure. There is currently no curative treatment for COPD and there is an urgent unmet need for new therapeutics that could modify the course of the disease. The mechanisms underlying COPD pathology are complex and are composed of chronic inflammatory processes, oxidative stress induced by continued exposure of the lungs to harmful particles and accelerated ageing due to an increased number of senescent cells within the airways. The main challenge of current studies is to explore how these underlying mechanisms coalesce to drive disease pathophysiology. This chapter aims to describe recent developments in our understanding of COPD mechanisms, from the inflammatory response to the induction of cellular senescence in the lung. Understanding these mechanisms may result in the development of new therapeutics that could be effective for COPD but also for other age-related diseases.
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Journal articlePrice E, Ahmad S, Althobiani MA, et al., 2024,
Development and evaluation of a tool to optimise inhaler selection prior to hospital discharge following an exacerbation of COPD
, ERJ OPEN RESEARCH, Vol: 10 -
Journal articleRitchie A, Singayagam A, Mitchell S, et al., 2024,
The Effect of Inhaled Corticosteroids on Pneumonia Risk in Patients With COPD-Bronchiectasis Overlap: A UK Population-Based Case-Control Study (vol 164, pg 875,2023)
, CHEST, Vol: 165, Pages: 754-754, ISSN: 0012-3692 -
Conference paperPillar A, Brown A, Daly K, et al., 2024,
Role and therapeutic manipulation of iron metabolism in asthma and influenza-A virus infection associated disease
, Publisher: WILEY, Pages: 27-27, ISSN: 1323-7799 -
Conference paperMahbub R, Tomassen M, Boedijono F, et al., 2024,
Impact of smoking on IL33 at transcriptomic and protein level
, Publisher: WILEY, Pages: 45-46, ISSN: 1323-7799 -
Conference paperCarroll O, Brown A, Mayall J, et al., 2024,
Female sex hormones modulate asthma severity by altering cellular metabolism
, Publisher: WILEY, Pages: 119-120, ISSN: 1323-7799 -
Journal articleWilliams P, Philip K, Buttery S, et al., 2024,
Immediate smoking cessation support during lung cancer screening: long-term outcomes from two randomised controlled trials
, Thorax, Vol: 79, Pages: 269-273, ISSN: 0040-6376Background: Immediate smoking cessation interventions delivered alongside targeted lung health checks (TLHC) to screen for lung cancer increase self-reported abstinence at three months. The impact on longer-term, objectively confirmed quit rates remains to established. Methods: We followed up participants from two clinical trials in people aged 55-75 years who smoked and took part in a TLHC. These randomised participants in the TLHC by day of attendance to either usual care (signposting to smoking cessation services) or an offer of immediate smoking cessation support including pharmacotherapy. In the QuLIT1 trial this was delivered face to face, in QuLIT2 it was delivered remotely. Follow up was conducted 12 months after the TLHC by telephone interview with subsequent biochemical verification of smoking cessation using exhaled CO. Results: 430 people were enrolled initially (115 in QuLIT1 315 in QuLIT2), with 4 deaths before 12 months leaving 426 [62.1±5.27 years old and 48% female] participants for analysis. At 12 months, those randomised to attend on smoking cessation support intervention days had higher quit rates compared to usual care adjusted for age, gender, deprivation, and which trial they had been in; self-reported 7-day point prevalence (20.0% vs 12.8%; AOR=1.78 95% CI, 1.04-2.89) and CO verified quits (12.1% vs 4.7%; AOR=2.97 95% CI, 1.38-6.90). Those in the intervention arm were also more likely to report having made a quit attempt (30.2% vs UC 18.5%; AOR 1.90 95% CI 1.15-3.15). Conclusion: Providing immediate smoking cessation support alongside TLHC increases long term, biochemically confirmed smoking abstinence.
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Journal articleWeng C-M, Wu W-C, Lee M-J, et al., 2024,
Influence of Staphylococcal enterotoxin-specific IgE sensitization on therapeutic efficacy of omalizumab therapy in severe asthma
, RESPIROLOGY, Vol: 29, Pages: 252-255, ISSN: 1323-7799 -
Journal articleButtery S, Lewis A, Alzetani A, et al., 2024,
Survival following Lung Volume Reduction procedures - results from the UK Lung Volume Reduction (UKLVR) Registry
, BMJ Open Respiratory Research, Vol: 11, ISSN: 2052-4439Introduction Lung volume reduction surgery (LVRS) and endobronchial valve (EBV) placement can produce substantial benefits in appropriately selected people with emphysema. The UK Lung Volume Reduction (UKLVR) registry is a national multicentre observational study set up to support quality standards and assess outcomes from LVR procedures at specialist centres across the UK.Methods Data were analysed for all patients undergoing an LVR procedure (LVRS/EBV) who were recruited into the study at participating centres between January 2017 and June 2022, including; disease severity and risk assessment, compliance with guidelines for selection, procedural complications and survival to February 2023.Results Data on 541 patients from 14 participating centres were analysed. Baseline disease severity was similar in patients who had surgery n=244 (44.9%), or EBV placement n=219 (40.9%), for example, forced expiratory volume in 1 s (FEV1) 32.1 (12.1)% vs 31.2 (11.6)%. 89% of cases had discussion at a multidisciplinary meeting recorded. Median (IQR) length of stay postprocedure for LVRS and EBVs was 12 (13) vs 4 (4) days(p=0.01). Increasing age, male gender and lower FEV1%predicted were associated with mortality risk, but survival did not differ between the two procedures, with 50 (10.8%) deaths during follow-up in the LVRS group vs 45 (9.7%) following EBVs (adjusted HR 1.10 (95% CI 0.72 to 1.67) p=0.661)Conclusion Based on data entered in the UKLVR registry, LVRS and EBV procedures for emphysema are being performed in people with similar disease severity and long-term survival is similar in both groups.
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