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Journal articleWang M, He Y, Hu H, et al., 2026,
Protective role of fatty acid oxidation against epithelial barrier dysfunction in allergic asthma.
, Redox Rep, Vol: 31BACKGROUND: Fatty acid oxidation (FAO) is implicated in lung diseases, but its role in bronchial asthma is not fully understood. We investigated its effect on airway epithelial barrier integrity. METHODS: Using a house dust mite (HDM)-induced murine asthma model and HDM, IL-4, IL-13, or TNF-α stimulated human primary bronchial epithelial cells (BECs) and bronchial epithelial (Beas-2b) cells, we modulated FAO with L-carnitine (agonist) and Etomoxir (inhibitor). BECs and Beas-2b cells were infected with lentivirus-mediated CPT1A shRNA prior to stimulation. Barrier function, mitochondrial oxidative stress, inflammation, and metabolism were assessed. RESULTS: FAO level in lungs negatively correlated with increased inflammation and tissue injury in HDM-induced asthmatic mice (all p < 0.05), while positively regulating tight junction protein expression. In BECs and Beas-2b cells, Etomoxir treatment and CPT1A knockdown exacerbated the impairment of FAO caused by various stimulants (all p < 0.05). Furthermore, FAO negatively regulated HDM/cytokine-induced epithelial barrier damage, hyperactive inflammatory response, and mitochondrial dysfunction in Beas-2b cells (all p < 0.05). In contrast, treatment with L-carnitine significantly alleviated these pathophysiological features in both in vivo and in vitro models. CONCLUSION: FAO plays a protective role in the occurrence and development of asthma by maintaining airway epithelial cell homeostasis and barrier function.
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Journal articleSaralaya D, Mustapa MN, Ferreira J, et al., 2026,
A phase 2a, double-blind, randomised, placebo-controlled trial of the myeloperoxidase inhibitor, mitiperstat, in participants with chronic obstructive pulmonary disease.
, Eur Respir JBACKGROUND: Neutrophilic inflammation is a common feature of chronic obstructive pulmonary disease (COPD). Mitiperstat, an inhibitor of myeloperoxidase expressed in neutrophils, may have potential as a COPD treatment. METHODS: This phase 2a, randomised, placebo-controlled, double-blind, parallel-arm, event-driven trial evaluated the efficacy and safety of mitiperstat 5 mg daily up to 24 weeks (NCT05492877). Adults (40-80 years) with moderate-to-severe COPD, at high risk of exacerbation, and receiving dual or triple inhaled therapy were included. The primary endpoint was time to first composite endpoint for exacerbations in COPD (COPDCompEx) event. Secondary endpoints included time to first moderate-to-severe COPD exacerbation, post-bronchodilator forced expiratory volume in 1 s (post-BD FEV1) change at Week 12, respiratory symptoms, disease impact and safety. RESULTS: Overall, 381 participants (mean age, 66.0 years; 39.6% female) were randomised to mitiperstat (n=189) or placebo (n=192). In total, 125 (66.1%) mitiperstat-treated versus 125 (65.1%) placebo-treated participants experienced COPDCompEx events over 24 weeks. There was no improvement in time to first COPDCompEx event (hazard ratio [HR] 1.07 [90% confidence interval (CI) 0.87, 1.32]; p=0.599) or time to first moderate-to-severe COPD exacerbation (HR 1.23 [90% CI 0.88, 1.73]) with mitiperstat versus placebo. Improvements in post-BD FEV1, respiratory symptoms or disease impact were not seen with mitiperstat. A similar proportion of participants in both groups reported adverse events; seven mitiperstat-treated participants and two placebo-treated participants had pneumonia during the study. CONCLUSION: These results indicate that the risks outweigh the benefits of mitiperstat as a treatment for COPD.
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Journal articleChae W, An J, Lee W, et al., 2026,
Circulating 1-Methylnicotinamide Predicts Dupilumab Response in Adult Asthma: A Prediction Model.
, Clin Exp Allergy, Vol: 56, Pages: 935-938Plasma 1‐methylnicotinamide is elevated in dupilumab responders, outperforming conventional type‐2 biomarkers. Combining 1‐methylnicotinamide with FeNO achieves the highest predictive accuracy for dupilumab treatment response.
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Journal articleKlimek L, Mullol J, Hummel T, et al., 2026,
The Unmet Need of Olfactory Testing in Inflammatory Disorders of the Upper Airways-An EAACI Position Paper.
, Allergy, Vol: 81, Pages: 2633-2655The sense of smell, with its extensive evolutionary history, is highly prone to disorders that can have a profound impact on daily life. Anosmia affects approximately 5% of the population, with an additional 15% exhibiting reduced olfactory function. The prevalence of olfactory dysfunction (OD) varies by population and age group, and standardized testing reveals a broad range of impacts. OD includes various causes, most commonly aging, inflammation of the olfactory epithelium, upper respiratory tract infections (URTI), traumatic brain injury, and neurological conditions. The recent COVID-19 pandemic has highlighted the association between viral infections and olfactory dysfunction, with severe hyposmia/anosmia being an early marker of infection. Despite its importance, the assessment of olfactory function remains inconsistent across clinical practices. Psychophysical smell tests, while vital for diagnosis and patient management, are underutilized, especially outside of specialized centers. Standardized testing methods are crucial for objective diagnosis, but significant challenges, including test variability, lack of comparability, and healthcare reimbursement issues, persist. The European Academy of Allergy and Immunology (EAACI) advocates for improvements in the quality and standardization of chemosensory assessments. Future efforts must prioritize education, incentives for better testing, and the integration of digital tools to expand access to olfactory testing and diagnosis in remote or quarantine situations. However, office-based testing remains irreplaceable, even with advancements in telemedicine.
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Journal articleBaylis S, Hopkinson NS, Feliu A, et al., 2026,
Statement of the European Respiratory Society on the tobacco endgame.
, Eur Respir J, Vol: 68 -
Journal articleShamji MM, Rider NL, Adcock I, et al., 2026,
PRACTALL 2025: Artificial intelligence-application of allergy and immunology to patient care.
, J Allergy Clin ImmunolArtificial intelligence (AI), first defined in 1955 by John McCarthy, has transformed daily life across industries through applications such as chatbots, autonomous vehicles, and navigation systems. The 2022 release of ChatGPT marked a pivotal moment, highlighting AI's rapidly expanding potential. The health care industry is increasingly embracing AI-enabled tools across oncology, pathology, and radiology to augment disease screening and clinical workflows. Ambient listening technologies support clinical documentation, reduce administrative burden, and improve patient-physician interactions. Large language models combined with natural language processing are being evaluated for generating clinical summaries managing patient portal messaging and converting freehand notes to electronic health records, while also uncovering patterns in patient data to support more personalized treatments. Forward-thinking health systems are establishing informatics departments to optimize these models. Notably, with 1 in 6 adults sourcing health information from AI, rising to nearly one-quarter among individuals younger than 30 years, there is a growing need to ensure that these technologies provide accurate and reliable information to safeguard patient safety and support appropriate clinical use. PRACTALL, a collaboration between the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy & Clinical Immunology, aims to equip allergist-immunologists with essential AI insights highlighting tools for clinical practice, education, and research. By addressing potential pitfalls and biases, PRACTALL illustrates how AI can enhance efficiency, improve patient care, and alleviate administrative burdens in health care.
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Journal articleSuh M, Oh J-Y, Won H-K, et al., 2026,
Patient-Anchored Cough Visual Analogue Scale and Leicester Cough Questionnaire Thresholds for Cough Control Classification in Chronic Cough.
, Lung, Vol: 204PURPOSE: The cough severity visual analogue scale (VAS) and the Leicester Cough Questionnaire (LCQ) are commonly used in chronic cough. While continuous scores are useful for tracking change, categorization is needed to define clinically relevant states. However, patient-anchored thresholds for cough control remain undefined. METHODS: Using the Korean Chronic Cough Registry (n = 890), we derived VAS and LCQ cutoffs anchored to a patient-reported cough control item. Receiver operating characteristic (ROC) analyses were performed using operational definitions of very well-controlled cough ("strongly agree" vs. all others), well-controlled cough ("strongly agree" + "agree" vs. all others), and uncontrolled cough ("disagree" + "strongly disagree" vs. all others). RESULTS: Both scores demonstrated stepwise gradients across cough control categories (p < 0.001). ROC-derived cutoffs for very well-controlled cough were VAS ≤ 10 (area under the curve [AUC], 0.911) and LCQ ≥ 15.8 (AUC, 0.877). For well-controlled cough, the corresponding cutoffs were VAS ≤ 30 (AUC, 0.866) and LCQ ≥ 15 (AUC, 0.856). For uncontrolled cough, the cutoffs were VAS ≥ 50 (AUC, 0.879) and LCQ ≤ 13.0 (AUC, 0.872). Cutoffs were consistent across newly referred chronic cough and refractory chronic cough subgroups. Concordance between VAS- and LCQ-derived classifications was moderate-to-substantial (weighted kappa = 0.55). CONCLUSION: Based on these findings, we propose a patient-anchored classification framework for cough control: very well-controlled cough (VAS ≤ 10, LCQ ≥ 16), well-controlled cough (VAS 11-30, LCQ 15.0-15.9), intermediate cough control (VAS 31-49, LCQ 13.1-14.9), and uncontrolled cough (VAS ≥ 50, LCQ ≤&th
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Journal articleShen J, Chaudhuri R, Bicknell S, et al., 2026,
The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.
, AllergySevere asthma is a heterogeneous disease. The mechanisms driving airway pathology when type 2 (T2) cytokine activity is suppressed remain poorly understood. This study aimed to provide insight by identifying the airway molecular pathways of T2 biomarker-high and -low severe asthma. We analysed clinical and transcriptomic data from bronchial biopsies and brushes in the UK Refractory Asthma Stratification Programme multi-centre severe asthma cohort (18 corticosteroid-resistant T2 biomarker-high [T2-high], 23 T2 biomarker-intermediate [T2-intermediate], 11 T2 biomarker-low [T2-low]) plus 20 healthy controls pre- and post-treatment with high-dose inhaled corticosteroids (ICS). Many genes dysregulated in asthma vs. health were concordantly dysregulated in healthy subjects receiving ICS. Severe asthma as a whole, independent of confounding by ICS, was characterised by upregulation of mucins, CEACAM5, typical T2-genes (POSTN, CLCA1, CCL26), epithelial mast cell genes, and CPA4. T2-high severe asthma demonstrated upregulated T2-dependent genes, epithelial barrier and keratin genes, adaptive immune responses, and impaired ciliary function. T2-low asthma showed upregulated Th1- and IL-17-associated genes (IDO1, CXCL10, GBP1, LAG3), interferon-γ signalling, neuroimmune pathways, airway smooth muscle-related genes, and neutrophil enrichment. T2-intermediate asthma exhibited a mixed molecular profile sharing features of T2-high and T2-low endotypes, with selective expression of the pathogen defence and antiviral response genes. The results were validated using bronchoscopy data from the U-BIOPRED Consortium. This study defines airway molecular endotypes of severe asthma associated with T2 biomarker high and low phenotypes, independent of corticosteroid effects. These findings offer insights for severe asthma management and the development of targeted biologic therapies.
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Journal articleBloom CI, Foer D, Aroda VR, et al., 2026,
It's more than mechanics: the case for metabolic endpoints in airways disease
, European Respiratory Journal, ISSN: 0903-1936 -
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.
, Thorax, Vol: 81, Pages: 758-765INTRODUCTION: 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 articleYang F, Seo S, Hasegawa T, et al., 2026,
Longer Asthma Duration Is Associated With Elevated Non-T2 Sputum Biomarkers and Reduced T2 Inflammation in Severe Asthma.
, AllergyBACKGROUND: Longer asthma duration predicts non-remission in Type-2 (T2) biologic-treated severe asthma, but underlying mechanisms remain unclear. We investigated associations between asthma duration and inflammatory biomarkers that may explain differential biologic response. METHODS: We analysed cross-sectional data from adults with severe asthma in U-BIOPRED. Asthma duration was defined as years from diagnosis to study entry. T2 and non-T2 biomarkers were measured in blood and sputum. Identical assays were performed in PRISM, a validation cohort of biologic-initiators. Multivariable regression models adjusted for age, sex, ethnicity, BMI, smoking and oral corticosteroid dose. Associations between duration-related biomarkers and 12-month biologic remission were explored in PRISM. RESULTS: In U-BIOPRED (n = 411), median asthma duration was 23 years (IQR 12-38). Longer duration was associated with higher non-T2 biomarkers including sputum CXCL9 (β = 0.024, 95% CI 0.011-0.038), sputum IL-6 (β = 0.024, 95% CI 0.011-0.037) and sputum neutrophils (β = 0.009, 95% CI 0.001-0.017), but lower T2 biomarkers including plasma periostin (β = -0.006, 95% CI -0.009 to -0.003), eosinophils (blood: β = -0.002, 95% CI -0.003 to -0.001; sputum: β = -0.023, 95% CI -0.035 to -0.011), sputum EDN (β = -0.032, 95% CI -0.049 to -0.014) and FeNO (β = -0.006, 95% CI -0.010 to -0.001). PRISM (n = 474) confirmed these associations. Higher sputum CXCL9 was associated with reduced remission in anti-IL-4Rα-treated patients with asthma duration ≥ 20 years (β = -1.73, 95% CI -3.180 to -0.276). CONCLUSION: Longer asthma duration was associated with elevated airway non-T2 inflammation and reduced systemic and airway T2 inflammation. This highlights the importance of airway bio
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Journal articleWang M, Hu H, Wang K, et al., 2026,
Deficiency of Mitochondrial Fatty Acid Enzyme, CPT1A, Underlies Airway Epithelial Barrier Dysfunction in Severe Asthma.
, AllergyBACKGROUND: Mitochondrial fatty acid oxidation through carnitine palmitoyltransferase-1A (CPT1A) leads to ATP generation. We examined its role in regulating permeability and mitochondrial metabolic homeostasis of airway epithelial cells in asthma. METHODS: Primary nasal epithelial cells (NECs) from healthy controls and severe asthma (SA) patients in air-liquid interface (ALI) were exposed to CPT1A siRNA/CPT1A overexpression lentiviral/L-carnitine (LCA). Epithelial TEER and FITC-dextran transport were measured. Bronchial biopsies from healthy and SA subjects and house dust mite (HDM) asthma mouse model were also studied. RESULTS: In NECs-ALI and in bronchial epithelial cells (BECs) from bronchial biopsies of SA, CPT1A expression was reduced compared to healthy controls. Knock-down of CPT1A in healthy NECs reduced expression of Occludin and E-cadherin and impaired epithelial barrier integrity (EBI), while upregulation of CPT1A with CPT1A overexpression lentiviral/LCA in SA-NECs increased the barrier proteins with improved EBI. CPT1A knockdown in healthy BECs increased release of mtROS, with mitochondrial disruption and activation of ERK1/2-NF-κB signaling pathway. These were aggravated with HDM exposure but N-acetyl-cysteine and MitoTempo reduced p-ERK1/2 and p-P65 activation, as well as EBI with CPT1A knockdown and HDM. In the mouse model, there was decreased airway epithelial CPT1A protein expression, associated with reduced airway hyperreactivity and inflammation, and in Occludin and ZO-1 expression, effects partly reversed by LCA, with restoration of mitochondrial integrity and EBI. CONCLUSION: CPT1A maintains epithelial barrier function through restoration of mitochondrial function in asthmatic airway epithelial cells. Restoration of deficient epithelial CPT1A of SA may represent a new treatment approach.
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Journal articleWawman RE, Shah PL, Boffito M, et al., 2026,
The relationship between plasma favipiravir concentrations and clinical outcomes in COVID-19
, ERJ Open Research, Vol: 12, ISSN: 2312-0541BackgroundFavipiravir has shown efficacy against SARS-CoV-2 in patients <60 years old, but data linking plasma concentrations to clinical outcomes are limited. This study investigated whether favipiravir plasma concentrations influence clinical efficacy and outcomes in patients hospitalised with COVID-19. The main research question was, How can antiviral dosing strategies be optimised to improve pandemic preparedness and treatment efficacy?MethodsAdult participants were drawn from the PIONEER trial, in which patients received oral favipiravir (1800 mg twice daily for 1 day, then 800 mg twice daily for 9 days) plus standard care. This analysis included patients with confirmed COVID-19 and ≥75% study adherence. Samples were collected between days 5 and 10 post-treatment initiation. The primary outcome was time to clinical improvement. Secondary outcomes included achievement of clinical improvement and mortality risk.ResultsOut of 140 patients (50% male; mean±sd age 59.5±14.8 years), target plasma concentrations were reached in 29 (21%). Mean time to improvement was 7.7±5.9 days in target achievers versus 9.1±7.2 days in non-achievers (p=0.26). The target was more often achieved in female (34%) than male (7%) participants (p=0.0002). Plasma concentration inversely correlated with body mass index (r= –0.4, p<0.0001), and with lower body mass index in achievers (26.0±5.1 kg·m−2 versus 30.5±6.9 kg·m−2, p=0.003). Alkaline phosphatase and alanine aminotransferase levels were also lower in achievers (p=0.004 and p=0.02, respectively).ConclusionMost patients did not reach target favipiravir levels. Concentrations were influenced by sex, body mass index and liver function, confirming the need for pharmacokinetically guided dosing and therapeutic monitoring to optimise antiviral efficacy in future pandemic responses.
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Journal articleChung KF, 2026,
From the London International Cough Symposium to the ERS Cough Conference: chronic cough comes of age.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541The @EuroRespSoc Cough Conference https://bit.ly/4asS7NF.
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Journal articleCarlsten C, Salvi S, Wong GWK, et al., 2026,
Supplements and medications for respiratory resilience against air pollution.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541Air pollution is a major threat to respiratory health. In this article, we review the current literature on accessible interventions that could help patients build resilience against this threat. We explore the potential benefits of antioxidant-rich diets, including supplements such as fish oil, vitamins C, D and E, and prebiotics, which have shown promise in reducing inflammation and oxidative stress, thereby mitigating air pollution-related respiratory decline. Nasal washes are commonly used to clear nasal passages, which could help to clear pollutants from the nasal passages and improve mucociliary clearance. Furthermore, medications such as nonsteroidal anti-inflammatory drugs and intranasal corticosteroids have been reported to reduce pollutant-related airway inflammation and lung function deterioration triggered by pollutant exposure. Given the generally favourable safety profile of these interventions, they are reasonable to consider in consultation with a care provider. Further research is needed to establish optimal dosing, safety and long-term efficacy, particularly for those exposed to chronic air pollution. Healthcare professionals should work together to further identify and implement effective interventions to mitigate the impact of air pollution on respiratory health.
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Journal articleKlimek L, Mullol J, Reitsma S, et al., 2026,
Correspondence: The First Biosimilar for Biologics in Allergy: CT-P39 (Omlyclo-Omalizumab-Igec) Is Available for Asthma, Chronic Spontaneous Urticaria, and Chronic Rhinosinusitis With Nasal Polyps.
, Allergy, Vol: 81, Pages: 2568-2570 -
Journal articleCecchi L, Annesi-Maesano I, Biagioni B, et al., 2026,
EAACI Guidelines on Environmental Science for Allergy and Asthma-Evidence-Based Recommendations for Prevention and Public Health Action to Mitigate the Impact of Pollen Exposure on Respiratory Allergy.
, AllergyDeveloped using the GRADE methodology, these EAACI guidelines provide evidence-based recommendations on the effectiveness of pollen reduction/avoidance strategies for allergic rhinitis (AR) and asthma, the utility of biomarkers for monitoring pollen-induced asthma and the efficiency of mitigation measures and of public health strategies. Systematic and narrative reviews and health economic analysis support the recommendations. According to GRADE, the certainty of evidence was moderate to very low, therefore conditional recommendations are provided to guide healthcare professionals, patients, and policymakers in developing personalized, preventive, and scalable interventions. Reducing/avoiding exposure to pollen should be recommended to reduce the risk of severe asthma exacerbations. Lung function decrease and exhaled nitric oxide increase may be predictive for pollen-induced asthma exacerbations. Real-time pollen monitoring and pollen concentration-based forecast may be recommended for managing pollen-induced AR and/or asthma. Pollutant information should be included in pollen information systems. Combined forecast (weather, pollen, pollutants) and warning systems might reduce the impact of thunderstorm asthma (TA). Emergency department/asthma-related services should be strengthened during pollen season and in TA. Personalized frameworks covering the types and allergenic potential of pollen, the coaggressors and the vulnerability of each patient are needed in daily practice. The fundamental role of prevention should be further prioritized.
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Journal articleAlzahrani A, Alghamdi S, Majrshi M, et al., 2026,
Use of oscillatory positive expiratory pressure (OPEP) devices to augment sputum clearance in COPD: an updated systematic review and meta-analysis
, Chronic Respiratory Disease, Vol: 23, ISSN: 1479-9723IntroductionEffective airway clearance is crucial in COPD management, and oscillatory positive expiratory pressure (OPEP) devices are a potential adjunct therapy for this. However, their clinical efficacy remains uncertain due to limited trial data.AimTo update our previous (2020) systematic review investigating the use of OPEP devices to augment sputum clearance in COPD.MethodsRandomised Clinical Trails s evaluating OPEP devices in COPD were identified from PubMed, CINAHL, Medline, Cochrane, and Embase (2020–2024). Outcomes included lung function, exercise capacity, exacerbations, and health-related quality of life (HRQoL), with pooled estimates calculated using random-effects models.ResultsTwelve trials (741 participants) were included. OPEP devices significantly reduced exacerbations (Odds Ratio: 0.39) and improved exercise capacity (+49 m at 6MWD). Small improvements were observed in FVC%, while HRQoL changes were not statistically significant. Accumulating evidence suggests benefits for sputum clearance and reduced antibiotic use. Devices were generally well accepted and safe.ConclusionOPEP devices appear to be safe and may reduce exacerbations, improve functional exercise capacity, and support sputum clearance in COPD.
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Journal articleBaraldi F, Mah JSY, Almuhanna A, et al., 2026,
Mucus Plug Formation is Associated with Eosinophilic Activation in Chronic Obstructive Pulmonary Disease.
, Am J Respir Crit Care Med -
Journal articleSong W-J, Kermani NZ, Versi A, et al., 2026,
Clinical Features of Cellular Senescence Pathways in Severe Asthma.
, AllergyBACKGROUND: Asthma severity increases with age, suggesting a role for accelerated biological ageing. We hypothesised that cellular senescence pathways such as the senescence-associated secretory pathway (SASP) and the p53-cellular senescence pathway are enriched in the airways of patients with severe asthma. METHODS: We utilised transcriptomic data from the U-BIOPRED cohort to analyse enrichment scores (ES) of p53 and SASP pathways in different airway compartments using gene set variation analysis. Findings in bronchial biopsies were validated in the independent NOVA cohort. We examined associations between senescence ES, clinical parameters and other asthma-related gene signatures. Functional clusters of the SASP gene set were also explored. RESULTS: In the U-BIOPRED cohort, p53 and SASP ES were significantly elevated in bronchial biopsies of severe asthmatics compared to mild-to-moderate asthmatics and healthy volunteers, with SASP enrichment validated in the NOVA cohort. In bronchial biopsies, higher senescence ES correlated with frequent exacerbations, oral corticosteroid use, comorbid nasal polyps and lower FEV1%. No significant enrichment was found in other airway samples according to asthma severity. In nasal brushings, SASP ES was significantly higher in participants with comorbid nasal polyps. A distinct SASP functional cluster related to lung injury and repair (Cluster 2) was strongly associated with clinical severity and nasal polyps. Senescence signatures correlated positively with oxidative phosphorylation and macrophage activation signatures, but not with eosinophil signatures. CONCLUSIONS: Cellular senescence pathways are enriched in severe asthmatic bronchial tissues and correlate with disease severity, remodelling and nasal polyps. These findings warrant further investigation into their therapeutic implications. TRIAL REGISTRATION: NCT01982162.
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