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Journal articleAnanth S, Wedzicha JA, 2026,
COPD exacerbations: Major events in the course of the disease
, PRESSE MEDICALE, Vol: 55, ISSN: 0755-4982 -
Journal articleLewis A, Jung P, Williams P, et al., 2026,
Singing for lung health following completion of pulmonary rehabilitation: feasibility of a randomised controlled trial.
, BMJ Open Respir Res, Vol: 13BACKGROUND: Pulmonary rehabilitation (PR) is a highly effective intervention for people with chronic respiratory disease; however, it is not known how best to sustain its benefits. Clinical trials are needed to establish if participation in singing for lung health (SLH) groups following PR will improve health-related quality of life, healthcare utilisation and exercise capacity compared with usual care. A feasibility study would help to guide development of these trials. METHODS: In a multicentre, mixed-methods randomised controlled feasibility trial, PR participants at four sites were prescreened at baseline assessment. An SLH taster session was included routinely as part of the PR programmes. Eligible PR completers were invited to take part in the trial and randomised to usual care or a 12-week SLH course. Feasibility outcomes included recruitment rate, intervention compliance (at least 8/12 sessions) and health economic analysis. Interviews with participants and study personnel were undertaken and thematic analysis of the results was completed. RESULTS: Between October 2022 and November 2023, 1311 patients were assessed to start PR, 838 completed. Of those completing, 243 were ineligible to take part (predominantly due to vaccination status and excluded diagnoses for PR referral), and 531 declined. 64 people (33 female, mean (SD) age 69 (12), 41 ethnically white, 33 with chronic obstructive pulmonary disease, 16 with asthma, 9 with interstitial lung disease, 6 with bronchiectasis) were recruited, with 30 (93.8%) SLH and 29 (90.6%) controls completing the study. 20 (62.5%) of the SLH group completed at least 8/12 SLH sessions. There was enthusiasm for a definitive trial from participants, clinicians and singing group leaders' perspectives, based on positive experiences of trial involvement. Improvements to recruitment strategy, intervention structure, outcome measures and staffing were suggested. CONCLUSIONS: A definitive randomised controlled trial of SLH post-PR
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Journal articleEvison M, Naylor R, Malcolm R, et al., 2026,
Health economic model to evaluate the cost-effectiveness of smoking cessation services integrated within lung cancer screening in the United Kingdom.
, ThoraxINTRODUCTION: Integrating smoking cessation supports into lung cancer screening can improve abstinence rates. However, healthcare decision-makers need evidence of cost-effectiveness to understand the cost/benefit of adopting this approach. METHODS: To evaluate the cost-effectiveness of smoking cessation interventions, and service delivery, we used a cohort-based Markov model, adapted from previous National Institute for Health and Care Excellence (NICE) guidelines on smoking cessation. This uses long-term epidemiological data to capture the prevalence of the smoking-related illnesses, updated through targeted literature searches as required from the core NICE model, with costs extracted from publicly recognised UK sources. RESULTS: All smoking cessation interventions appeared cost-effective at a threshold of £20 000 per quality-adjusted life year, compared with no intervention or behavioural support alone. Offering immediate smoking cessation as part of lung cancer screening appointments, compared with usual care (onward referral to stop smoking services), was also estimated to be cost-effective with a net monetary benefit of £2198 per person, and a saving of between £34 and £79 per person in reduced workplace absenteeism among working age attendees. Estimated healthcare cost savings were more than four times greater in the most deprived quintile compared with the least deprived, alongside a fivefold increase in quality adjusted life years accrued. CONCLUSIONS: Smoking cessation interventions within lung cancer screening are cost-effective and should be integrated, so that treatment is initiated during screening visits. This is likely to reduce overall costs to the health service, and wider integrated care systems, improve quality and length of life, and may lessen health inequalities.
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Journal articlede Santana MBR, Cruz AA, De Araujo JLF, et al., 2026,
Variants in the Glucocorticoid Receptor gene (NR3C1), asthma control and serum cytokine levels
, Respiratory Medicine, Vol: 251, ISSN: 0954-6111IntroductionAsthma is a heterogeneous disease usually treated with inhaled corticosteroids (ICS) and long-acting beta2 agonists. However, not all individuals achieve adequate control with ICS.AimTo identify genetic variants in the glucocorticoid receptor gene (NR3C1) associated with asthma endophenotypes, bronchodilator reversibility, and asthma control under medium-to-high ICS doses.MethodsAssociation analyses were performed in 365 patients with moderate-to-severe asthma, 383 with mild asthma, and 330 non-asthmatic individuals. Asthma severity was defined by the need for regular treatment with medium-to-high ICS doses. Bronchodilator reversibility was defined as an increase of ≥200 ml and ≥12 % in FEV1 from baseline. Asthma control was assessed using the ACQ6 score. Serum cytokine concentrations were measured with Luminex.ResultsThe A allele of rs2918417 was associated with reduced risk of moderate-to-severe asthma (OR: 0.50; 95 % CI: 0.26–0.98) and fewer exacerbations (OR: 0.54; 95 % CI: 0.30–0.96); GA/AA genotypes showed lower IL-8 and IL-13 levels compared to GG. The G allele of rs6877893 decreased the risk of uncontrolled asthma in the recessive model (OR: 0.53; 95 % CI: 0.29–0.98), with GG carriers showing reduced IL-17A. Conversely, the A allele of rs4585488 increased risk of uncontrolled asthma (OR: 4.42; 95 % CI: 1.06–18.48), and the C allele of rs4912650 was linked to poor control (OR: 1.64; 95 % CI: 1.01–2.69). The G allele of rs4607376 was associated with lack of bronchodilator reversibility (OR: 1.51; 95 % CI: 1.05–2.17) and asthma exacerbations (OR: 1.37; 95 % CI: 1.01–1.87).ConclusionsNR3C1 variants are associated with moderate-to-severe asthma, poor control, lack of bronchodilator reversibility, and differential cytokine profiles.
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Journal articleFeleszko W, Caminati M, Gern JE, et al., 2026,
Effect of tezepelumab on asthma exacerbations co-occurring with infection-attributed acute respiratory illnesses.
, Ann Allergy Asthma Immunol, Vol: 136, Pages: 61-65.e1BACKGROUND: Tezepelumab, a human monoclonal antibody, blocks the activity of thymic stromal lymphopoietin. In the phase 2b PATHWAY (NCT02054130) and phase 3 NAVIGATOR (NCT03347279) studies, tezepelumab reduced exacerbations and improved lung function, asthma control, and health-related quality of life vs placebo in patients with severe, uncontrolled asthma. OBJECTIVE: To evaluate the incidence of asthma exacerbations co-occurring with documented acute respiratory illnesses attributed to infections. METHODS: Patients were randomized 1:1 to receive tezepelumab 210 mg subcutaneously or placebo every 4 weeks for 52 weeks. The incidence of asthma exacerbations co-occurring with respiratory illness-related adverse events (AEs) was assessed. Co-occurrence was defined as at least 1 day of overlap between a respiratory illness-related AE and the asthma exacerbation period beginning 7 days before the start of the exacerbation until the end of the asthma exacerbation. RESULTS: Of the 1334 patients (tezepelumab, n = 665; placebo, n = 669) included, 312 experienced at least 1 asthma exacerbation co-occurring with a respiratory illness-related AE attributed to an infection. The incidence of asthma exacerbation co-occurring with a respiratory illness-related AE was lower in the tezepelumab group than in the placebo group overall (18.2% vs 28.6%; exposure-adjusted incidence difference [EAID], -11.1 [95% CI: -15.75, -6.41]) and among patients with perennial allergy (EAID, -11.6 [95% CI: -17.44, -5.69]) and without perennial allergy (EAID, -10.2 [95% CI: -18.16, -2.10]). CONCLUSION: Tezepelumab reduced asthma exacerbations attributed to respiratory infections in patients with severe, uncontrolled asthma compared with placebo, irrespective of perennial allergy status. TRIAL REGISTRATION: This is a pooled analysis of 2 studies registered at Clinicaltrials.gov: PATHWAY (NCT02054130) and NAVIGATOR (NCT03347279).
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Journal articleSousa-Pinto B, Louis R, Anto JM, et al., 2025,
Adherence to inhaled corticosteroids and long-acting β2-agonists in asthma: A MASK-air study
, PULMONOLOGY, Vol: 31, ISSN: 2531-0437- Cite
- Citations: 11
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Journal articleNamporn T, Manopwisedjaroen S, Ngodngamthaweesuk M, et al., 2025,
Evidence of Mpox clade IIb infection in primary human alveolar epithelium
, EMERGING MICROBES & INFECTIONS, Vol: 14 -
Journal articlePham DD, Kwon H-S, Song W-J, et al., 2025,
Type 2 Biomarkers as Mediators of Clinical Remission With Biologics in Severe Asthma
, ALLERGY, ISSN: 0105-4538 -
Journal articleWilliams P, Buttery S, Perkins A, et al., 2025,
Exploring the predictors and barriers to accepting smoking cessation support within a targeted lung health check setting
, BMJ Open Respiratory Research, ISSN: 2052-4439Background: The Quit Smoking Lung Health Intervention Trials (QuLIT-1 and -2) and other studies show that providing immediate smoking cessation within lung cancer screening services substantially improves quit rates. However, in the QuLIT2 trial only around half of those offered smoking cessation support actually accepted it. Understanding what underpins this and how to facilitate higher smoking cessation rates would enhance the health impact of the Targeted Lung Health Check programme.Method: We compared characteristics of participants in the intervention arm of the QuLIT-2 study who accepted or declined the offer of smoking cessation support and conducted thematic analysis of interviews with 15 smokers who had declined it. Results: Of 152 randomised to smoking cessation support (61.3±4.8 years, 42% female), 80 declined the offer and 15 dropped out after the initial session leaving 57 “accepters”. Accepters were more likely to be female [53% vs 40% AOR: 3.30, 95%CI 1.47-7.48], younger [AOR: 0.90(0.80-0.98)] and were more likely to live in areas of medium or low deprivation, [AOR: 5.30(1.86-22.85)]. Thematic analysis of the interviews revealed four main barriers to acceptance: concerns about mental health, beliefs about quitting smoking and about the effectiveness of interventions, and negative past experiences of smoking cessation support.Discussion: Cessation services embedded in lung screening clinics need to anticipate barriers such as mental health concerns, past experiences and personal beliefs. Efforts should be made to design and offer equitable services that meet the needs of this population. Trial registration: This study is registered online: ISRCTN12455871.What is already known on this topic- Intensive smoking cessation support embedded within lung cancer screening services significantly increases 3 and 12 month quit rates among this high-risk population. What this study adds- Despite the success of cessation embedded into screening, a
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Journal articleBloom C, Yang F, Mcclean M, et al., 2025,
Global prevalence of eligibility for biologic therapy in ATS/ERS-defined severe asthma: A Systematic Review
, World Allergy Organization Journal, ISSN: 1939-4551 -
Journal articleAntao J, Rodrigues G, Zounemat-Kermani N, et al., 2025,
Proteomic and Transcriptomic Signatures of Poor Asthma Symptom Control in the U-BIOPRED Cohort
, ALLERGY, ISSN: 0105-4538 -
Journal articleTahmasebi S, Amani D, Adcock IM, et al., 2025,
Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential
, Cancer Cell International, ISSN: 1475-2867Non-small cell lung cancer (NSCLC) is responsible for most lung cancer diagnoses and causes elevated worldwide mortality rates, mostly due to late detection and the development of resistance against medicines. This review summarizes evidence regarding miR-145, a downregulated NSCLC microRNA, and emphasizes the multifaceted tumor-suppressor activity of miR-145 involving the repression of oncogenes such as c-Myc, epidermal growth factor receptor (EGFR), and octamer-binding transcription factor 4 (OCT4) to restrict cell growth, stemness, epithelial-to-mesenchymal-transition (EMT), metastasis via Phosphoinositide 3-kinases (PI3Ks)/ activation of protein kinase B (AKT, Mitogen‑activated protein kinase (MAPK), and transforming growth factor beta (TGF-β)/Smad signaling. miR-145 also exhibits potential diagnostic specificity in distinguishing NSCLC cases from controls through serum/plasma testing, with greater sensitivity/specificity in multi-miRNA sets, and prognostic value predicting resistance, survival, and disease advancement. Therapeutically, miR-145 enhances responses to chemotherapies, targeted therapies, radiotherapy, and immunotherapies by counteracting resistance networks. Utilizing novel delivery platforms, such as nanoparticles, exosomes, and chemical modifications, may overcome stability and targeting issues that exist with miRNA therapies. Through the integration of preclinical and clinical information, this review helps identify crucial research gaps, such as incompletely defined regulatory networks and the need for large-scale studies, and calls for the application of advanced techniques to expedite the integration of miR-145-based treatments with personalized NSCLC therapy for improved outcomes.
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Journal articleFeng Y, Weng J, Li C, et al., 2025,
FUNDC1 promoted ferroptosis via JNK pathway in cigarette smoking-induced chronic obstructive pulmonary disease
, Lung, Vol: 203, ISSN: 0341-2040BackgroundCigarette smoking (CS), the major risk factor for chronic obstructive pulmonary disease (COPD), induces oxidative stress, mitophagy, and ferroptosis. Because FUN14 domain-containing protein 1 (FUNDC1), a mitophagy receptor, may drive the onset and progression of COPD, we investigated its role in CS-induced ferroptosis in COPD and to explore the underlying cellular signaling mechanisms.MethodsWild-type (C57BL/6J background) and FUNDC1-knockdown (KD) mice were exposed to CS for 12 weeks. FUNDC1-KD and FUNDC1-overexpressing (OE) alveolar epithelial A549 cells were exposed to CS extracts (CSE) in the presence and absence of the JNK inhibitor, SP6001 (10 mM). Oxidative stress, inflammation, mitochondrial function, and ferroptosis were measured.ResultsFUNDC1 expression was increased in lung tissues from COPD patients and CS-exposed mice. CS exposure induced airway inflammation, reduced lung function, and enhanced ferroptosis in mice. FUNDC1-KD prevented CS-induced lung injury in mice. Similarly, CSE exposure up-regulated FUNDC1 expression, promoted ferroptosis, inflammation, oxidative stress, lipid peroxidation, and mitochondrial damage in A549 cells. FUNDC1-KD prevented CSE-induced cellular damage. Transcriptomic data indicated that FUNDC1 mediated ferroptosis through the JNK pathway. These in vitro results were further confirmed by pretreatment with the JNK inhibitor SP6001.ConclusionFUNDC1 plays an important role in CS-exposed alveolar epithelial cells and in a mouse model of COPD through the JNK-ferroptosis pathway.
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Journal articleAlimohammadi M, Amani D, Adcock IM, et al., 2025,
Dual role of mir-146a in non-small cell lung cancer progression: molecular mechanisms and clinical potential
, Cellular Signalling, Vol: 136, ISSN: 0898-6568Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality. 2.48 million new cases were reported globally in 2022, driven by rising adenocarcinoma rates linked to environmental factors such as air pollution. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by targeting messenger RNA for degradation or translational repression. Emerging studies highlight miR-146a as a molecular pivot with dual functionality that acts as a tumor suppressor by inhibiting NF-κB signaling to reduce inflammation and chemoresistance while paradoxically exhibiting oncogenic potential through immune modulation in specific microenvironments. The expression of miR-146a has been associated with numerous pathological and physiological alterations in cancer cells, including the modulation of various signaling pathways such as TNF-α, NF-κB, MEK-1/2, and JNK-1/2. miR-146a can act exogenously through extracellular vesicles and thereby reprogram tumor-associated macrophages to either promote or inhibit metastasis depending on cellular context. The diagnostic potential of miR-146a is underscored by expression patterns correlating with disease progression and treatment response in NSCLC, whilst preclinical studies suggest therapeutic promise when combined with checkpoint inhibitors. In this review, we first discuss the biogenesis and function of miR-146a in NSCLC development, with emphasis on recent findings that underscore the dual role of miR-146a in the regulation of cell proliferation, invasion, inflammation, immune responses, and chemoresistance in NSCLC. We also describe the possible function of miR-146a as a biomarker for cancer diagnosis, prognosis, and therapeutic target.
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Journal articleSousa-Pinto B, Schleich F, Louis G, et al., 2025,
Daily digital biomarkers in the follow-up and clustering of patients with asthma
, Pulmonology, Vol: 31, ISSN: 2531-0429Background and Research questionWe aimed to assess whether levels of digital biomarkers can reflect monthly patterns of asthma controlStudy design and methodsWe performed a longitudinal study on patients with asthma and comorbid rhinitis who filled ≥26 days of data in a month in the MASK-air® app and who reported at least 1 day of treatment with an inhaled corticosteroid with or without a long-acting β2-agonist (ICS ± LABA). We applied k-means cluster analysis to define clusters of months according to daily asthma control and medication use. Clusters were compared using digital biomarkers (visual analogue scale [VAS] on asthma symptoms and electronic daily asthma control score [e-DASTHMA]). We compared patients who did not switch with patients who switched their ICS ± LABA.ResultsWe assessed 243 patients and 1358 months. We identified three clusters of poor asthma control despite high ICS ± LABA adherence, one cluster of poor asthma control and poor ICS ± LABA adherence, one cluster of good asthma control and high ICS ± LABA adherence and one cluster of good asthma control despite poor ICS ± LABA adherence. These clusters displayed relevant differences in VAS asthma and e-DASTHMA levels. Similar clusters were found in ‘non-switchers’ versus ‘switchers’.ConclusionLevels of digital biomarkers reflect asthma control patterns and might be used to monitor patients with asthma.
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Journal articleMazzone SB, Chung KF, Cho PSP, et al., 2025,
Future directions for clinical and research development in chronic cough
, Ers Monograph, Vol: 2025-December, Pages: 317-325, ISSN: 2312-508XThis Monograph provides a comprehensive review of CC, highlighting significant progress in the field over recent years. The contributing chapters also demonstrate key future directions that warrant attention. This includes reclassifying cough, for example into chronic primary cough and chronic secondary cough, to reflect that it can be both a disease and a symptom; developing new diagnostic tools and biomarkers to identify specific CC endotypes based on different underlying mechanisms; creating targeted therapies for these endotypes; improving clinical trial design with better endpoints and digital monitoring tools; and expanding our understanding of the full patient burden. Effective progression of these future priority areas will benefit from greater efforts to incorporate patient perspectives. There is also an additional and distinct need for research investigating CC in children, as much of our current understanding comes from studies in adults. Addressing these future directions will progress the field further towards effective management strategies for patients impacted by CC.
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Journal articleChung KF, Song WJ, 2025,
Use of digital monitoring technologies to measure chronic cough: “cough-omics”
, Ers Monograph, Vol: 2025-December, Pages: 296-305, ISSN: 2312-508XObjective measurement of cough frequency has been developed over the past 25 years. Current cough monitors are semi-automatic, limited to 24 h recordings using microphone detection and portable sound recorders, and have provided valuable information on cough frequency in patients with CC, which is modestly correlated with patient-reported outcomes. Their main use at the current time is in clinical trials for assessment of novel antitussives. Automatic analysis of cough events using machine learning has allowed for the use of digital tools and devices that in turn has led to the continuous unobtrusive recordings over long periods of time. The process of “cough-omics”, which is the analysis of large amount of data thus derived, has shown wide variability of daily cough counts in CC at an individual level and the lack of predictability of the cough counts in some for monitoring the effects of antitussives. There will be a greater understanding of the pathophysiology of cough with the analysis of cough-omics on how to use these new monitors efficiently both for clinical trials and in the clinic.
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Journal articleSong WJ, Chung KF, 2025,
Recent developments in the antitussive area
, Ers Monograph, Vol: 2025-December, Pages: 306-316, ISSN: 2312-508XRecent advances in CC research have led to a shift in perspective, with RCC and UCC recognised as forms of CHS. This condition is characterised by maladaptive sensitisation in both peripheral and central neural pathways. Key peripheral targets include transient receptor potential (TRP) channels, voltage-gated sodium channels, and purinergic (P2X3) receptors. Central mechanisms have been revealed through neuroimaging studies and clinical responses to neuromodulators, such as gabapentin and low-dose opioids. The clinical development of gefapixant, a P2X3 antagonist, validated the P2X3-ATP pathway as a therapeutic target, although limitations (e.g. taste disturbances and modest efficacy) led to the exploration of more selective agents. Emerging therapies include more selective P2X3 antagonists, TRPM8 agonists, neurokinin-1 receptor antagonists, N-methyl-D-aspartate receptor blockers, and novel opioid receptor modulators like nalbuphine. However, several challenges remain, including the lack of validated in vitro and in vivo experimental models, and limited access to nerve tissues. The heterogeneity of underlying mechanisms also complicates trial outcome and supports the need for better patient stratification. Furthermore, large placebo effects and the limitations of current efficacy end-points, such as 24-h cough frequency, hinder the detection of meaningful treatment effects. Future research must focus on identifying reliable biomarkers, refining trial methodologies and tailoring therapies to specific patient subgroups to improve CC treatment outcome.
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Journal articleSong WJ, McGarvey L, Cho PSP, et al., 2025,
Introduction
, Ers Monograph, Vol: 2025-December, Pages: x-xiii, ISSN: 2312-508X -
Journal articleAli N, Katsouli J, Auyang E, et al., 2025,
Microplastic and nanoplastic pollution and associated potential disease risks
, The Lancet Planetary Health, Vol: 9, ISSN: 2542-5196Microplastics and nanoplastics (MNPs) are emerging pollutants widely dispersed in the environment, with humans primarily exposed through ingestion and inhalation. Although their biological effects are being increasingly studied, their potential effect on human health and disease risk remains uncertain. This Review summarises evidence on potential disease risks of human exposure to MNPs, while highlighting key limitations and research gaps. Evidence suggests that MNP exposure might elevate the risk of various diseases, including metabolic, respiratory, cardiovascular, neuroendocrine, hepatic, renal, and skin disorders, as well as infectious diseases, cancer, and ageing-related disorders. Despite extensive evidence of adverse effects in animal models and cell cultures, direct evidence linking MNP exposure to human disease risk remains scarce. A key challenge on research of MNPs lies in the scarcity of robust human exposure data and the narrow scope of existing studies on specific types of MNPs, leaving several environmentally prevalent plastic particles understudied. Addressing these gaps will require investigating the mechanisms of toxicity, relevant biomarkers, and disease pathways associated with MNP exposure. Such efforts will be essential to clarify human health risks and inform future regulatory and mitigation strategies.
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