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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 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 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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Journal articleHopkinson N, 2026,
Effect of Dietary Nitrate Supplementation on Exercise Performance in Hypoxic IPF (EDEN-OX3): a double-blind, placebo-controlled, randomised crossover study
, Thorax, ISSN: 0040-6376Dietary nitrate (NO₃⁻) supplementation has been shown to improve vascular function and exercise capacity in COPD and in pulmonary hypertension. In a double-blind, placebo-controlled cross-over study in 20 patients with idiopathic pulmonary fibrosis who desaturated on exercise, endurance shuttle walk test improved by a median[IQR] difference of 31s [–9.5 to 100.0;(p=0.043], following a single dose of 140mls nitrate rich beetroot juice, as did brachial artery flow mediated dilatation; +4.25% (95% CI: –0.71 to 8.45; p=0.036), compared to following placebo nitrate depleted placebo juice. Longer-term studies are needed to see if these acute effects translate into sustained benefit.
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Journal articleWilliams PJ, Hopkinson NS, 2026,
The 2026 Tobacco and Vapes Act: on to the tobacco endgame.
, Thorax, Vol: 81, Pages: 635-637 -
Journal articleKinoshita R, Sathyapala A, Polkey MI, 2026,
Has the time come for workplace screening for obstructive sleep apnoea (OSA)?
, Thorax, Vol: 81, Pages: 638-641 -
Journal articleHopkinson NS, 2026,
A London Lark Rising: the story of the people and places of the East India Company.
, BMJ, Vol: 393 -
Journal articlePhilip K, Buttery S, Hopkinson N, et al., 2026,
The relationship of breathlessness with social isolation and loneliness: a nationally representative cohort study of older adults in England
, BMJ Public Health, ISSN: 2753-4294Introduction Breathlessness is a common and distressing symptom impacting quality of life and limiting activities of daily living. Social isolation and loneliness are associated with increased morbidity and mortality, being problems in themselves and risk factors for poor health. Qualitive studies indicate breathlessness impacts social health, however quantitative evaluation is limited. We aimed to assess the relationship of breathlessness with social isolation and loneliness in adults. Methods Using a nationally representative sample of older adults aged ≥50years from the English Longitudinal Study of Ageing (N=6,623). The sample had 44% males, mean age of 70years (SD=10). We examined associations of baseline breathlessness (mMRC breathlessness scale) with loneliness (3-item UCLA loneliness scale) and social isolation (low social contact, low community participation, living alone), at baseline, and follow-up at 4- and 8-years later, using regression models adjusted for confounders. Results At baseline, breathlessness was associated with higher levels of loneliness (coef.=0.161, 95%CI 0.1130.209), and social isolation, including low social contact (coef.=0.094, 95%CI 0.028-0.159), low community participation (coef.=0.169, 95%CI 0.117-0.221), and living alone (OR 1.089, 95%CI 1.0261.157). Longitudinally, breathlessness was associated increasing loneliness and reducing social contact and community participation at 4 and 8-year follow-up. Breathlessness was not associated with change in living alone. Findings were independent of identified confounders. Conclusions Breathlessness is related to increasing social isolation and loneliness, potentially due to limiting the amount and quality of social interactions. These findings suggest important psychosocial impacts of breathlessness requiring holistic management strategies.
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Journal articleButtery SC, Barraclough R, Batchelor TJP, et al., 2026,
Establishing the top ten research priorities for lung volume reduction treatment for people with COPD
, Thorax, ISSN: 0040-6376Lung volume reduction procedures are an established evidence-based aspect of chronic obstructive pulmonary disease (COPD) care. We conducted a research prioritisation exercise involving people with COPD and healthcare professionals across a range of disciplines, to identify a clear set of 10 questions to guide the development of research proposals in this area. Priorities were identified using an iterative approach based on the James Lind Alliance methodology. The final set of 10 priorities address the identification, assessment and optimisation of patients with COPD prior to any procedure, how lung volume reduction procedures are conducted and how care after the procedure has taken place should be organised.
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Journal articleBloom CI, 2026,
When the reliever becomes the risk.
, Thorax -
Journal articleMacLeod MA, Knott KD, Nicol ED, et al., 2026,
Reply to Liu et al.: Considerations on stratified analysis and biomarker use in coronary artery disease detection in chronic obstructive pulmonary disease.
, Am J Respir Crit Care Med, Vol: 212, Pages: 1368-1369 -
Journal articleBertels X, Scadding GK, Backer V, et al., 2026,
Shaping the Future of Respiratory Care: A Look Into the Next Decade and Strategic Recommendations by the European Forum for Research and Education in Allergy and Airways Diseases.
, Chest, Vol: 169, Pages: 1641-1652Chronic respiratory diseases (CRDs) remain 1 of the leading causes of preventable morbidity and disability worldwide, affecting up to one-third of the total Western population in 2025. Recognizing the substantial burden of inflammatory airway diseases such as asthma, COPD, chronic rhinosinusitis, and respiratory allergy, the European Forum for Research and Education in Allergy and Airway Diseases (EUFOREA) organized the symposium "Shaping the Future of Respiratory Care" in April 2025 in Brussels, Belgium, at the occasion of the 10-year jubilee. Featuring keynote speakers from the World Health Organization and EUFOREA, this initiative had the following aims: (1) promoting dialogue on translating innovations into daily clinical practice; (2) encouraging collaboration between the different stakeholders in the respiratory field; and (3) defining strategic priorities to transform respiratory care and arrest the CRD epidemic over the next decade. The symposium highlighted the importance of moving toward predictive, preventive, and patient-centered medicine, while supporting value-based health care systems to improve long-term patient outcomes. This report summarizes the main insights and strategic directions discussed at the meeting.
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Journal articleKocks JWH, Harrison T, Bell JP, et al., 2026,
Global pMDI Use and the Potential Impact of European PFAS Legislation on Access to These Essential Inhaled Medications.
, Pulm Ther, Vol: 12, Pages: 653-666INTRODUCTION: Many essential inhaled medicines recommended in guidelines are delivered to the lung via pressurized metered-dose inhalers (pMDIs). Global environmental legislation will lead to phasing out of hydrofluoroalkane propellants currently used in pMDIs, owing to their global warming potential (GWP). Furthermore, the European Chemicals Agency is reviewing proposed legislation to ban per- and polyfluoroalkyl substances (PFAS) on the basis of chemical structure, which could also impact pMDI availability. Here, we estimated pMDI use as a proportion of all inhaler use in 60 countries, spanning six geographical regions, to understand the relevance of any pMDI restrictions to patients and prescribers. METHODS: pMDI use as a percentage of total inhaler use during 2022 was calculated by country and geographical region using inhaler sales data (a surrogate of use) from the IQVIA Quarterly MIDAS database; inhaler use for the 10-year period from 2013 to 2022 was also evaluated for these regions. Data were compared by individual inhalations. The total patient population living with asthma and/or chronic lower respiratory disease was calculated on the basis of Eurostat (the statistical office of the European Union [EU]) 2019 data and available disease prevalence statistics. Maintenance pMDI utilization was estimated by adjusting for ratio of maintenance pMDI use to total inhaler use. RESULTS: Across all countries analyzed, pMDIs accounted for the largest proportion of inhaler use in 2022 (77.3%). In 51 out of 55 countries with available country-level data, pMDIs represented > 50% of total inhaler use. After adjusting for pMDI usage, an estimated 8.1 million EU patients received a maintenance pMDI in 2022, with the greatest proportion in Germany and France. CONCLUSIONS: pMDIs are vital inhalers for most patients in Europe and around the world. While transitioning to near-zero or low-GWP inhalers, it is essential to avoid unintended consequences from the pr
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Journal articleWon H-K, Lee J, Yun JW, et al., 2026,
Synergistic Induction of Neutrophilic Inflammatory Programs by Staphylococcus aureus and Cigarette Smoke in Airway Epithelial Cells.
, Immune Netw, Vol: 26, ISSN: 1598-2629Staphylococcus aureus (SA) colonization and cigarette smoking are both implicated in the pathogenesis of chronic airway disease, yet their combined effects on epithelial responses remain unclear. We investigated transcriptomic changes in human bronchial epithelial cells (BEAS-2B) following co-exposure to SA and cigarette smoke extract (CSE). RNA sequencing revealed that combined SA+CSE co-exposure was associated with a marked increase in differentially expressed genes, compared with single exposures. Functional enrichment and network analyses identified significant activation of pathways related to neutrophil migration, extracellular matrix remodeling, and inflammatory cascades, including TNF and IL-17 signaling. Key hub genes, notably CCL20, CXCL1, CXCL8, and IL-24, showed marked synergistic upregulation, which was validated by quantitative RT-PCR. These findings suggest that SA and cigarette smoke co-exposure is associated with a transcriptomic profile suggestive of neutrophilic inflammation. The involvement of IL-24 and IL-17 signaling suggests potential pathways linking bacterial colonization and smoking to airway inflammation and remodeling.
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Journal articlePortacci A, Ventura L, Menzella F, et al., 2026,
Small Airway Dysfunction May Mediate the Association Between Body Mass Index and Severe Asthma Exacerbations.
, Eur Respir JBACKGROUND: Obesity is associated with poorer asthma outcomes and an increased risk of exacerbations, but the underlying mechanisms remain incompletely understood. Small airway dysfunction (SAD) may represent a key mechanistic link between excess body weight and adverse asthma outcomes. METHODS: In this multicenter observational study, adult patients with asthma underwent clinical characterization, spirometry and impulse oscillometry (IOS). SAD was defined using a composite criterion based on peripheral airway resistance (R5-20), reactance area (AX) and the ratio of peripheral to total airway resistance (R5-20)/R5. Associations between body mass index (BMI), SAD and severe asthma exacerbations were assessed using multivariable regression models. Non-linear relationships were explored using generalized additive models and mediation analyses quantified the contribution of SAD to the obesity-exacerbation association. FINDINGS: Among 1169 patients, IOS-defined SAD was significantly more prevalent in individuals with BMI≥30 kg·m-2. Increasing BMI was associated with worse oscillometric parameters (p<0.0001), following a non-linear pattern with steeper deterioration beyond BMI values of approximately 28-30 kg·m-2. SAD was independently associated with obesity (adjusted OR 2.11, 95% CI 1.56-2.86) and with severe asthma exacerbations in the previous year (adjusted OR 2.01, 95% CI 1.53-2.65, both p<0.0001). Mediation analyses showed that SAD accounted for 26%-41% of the association between obesity and exacerbation risk (p=0.004 and 0.03). Spirometric indices provided limited additional information. INTERPRETATION: Oscillometry-defined small airways dysfunction (SAD) represents a non-linear functional trait underlying the association between obesity and severe asthma exacerbations, supporting its clinical relevance in obese patients with asthma and identifying SAD as a potential treatable trait.
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