European Respiratory Journal最新文献

{"title":"Attacking asthma - viruses and azithromycin: connecting the mechanistic dots.","authors":"Vanessa M McDonald, Peter G Gibson","doi":"10.1183/13993003.01038-2026","DOIUrl":"https://doi.org/10.1183/13993003.01038-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating mental health into respiratory care: reflections on the ELF/ERS mental health statement and advocacy pack.","authors":"Ingeborg Farver-Vestergaard, Ben Ainsworth, Latinka Basara, Jeanette Boyd, Lisa Jane Brighton, Jean-Marie Bruzzese, Jean-Michel Fourrier, Markus C Hayden, Ann Hutchinson, Samantha Piers, Liz Steed, Marieke Verkleij, Eleonora Volpato, Laura Wilde, Andreas von Leupoldt","doi":"10.1183/13993003.01146-2026","DOIUrl":"https://doi.org/10.1183/13993003.01146-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GOLD stage 1 COPD requires precise intervention based on disease progression.","authors":"Fan Wu, Qi Wan, Xiaohui Wu, Kunning Zhou, Junfeng Lin, Yumin Zhou, Nanshan Zhong, Pixin Ran","doi":"10.1183/13993003.01006-2026","DOIUrl":"https://doi.org/10.1183/13993003.01006-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Azithromycin enhances epithelial antiviral immunity in uncontrolled asthma: results from the AZIMUNE randomised controlled trial.","authors":"Muzhda Ghanizada, Sofia Malm Tillgren, Mandy Menzel, Louis Praeger-Jahnsen, Nihaya Mahmoud Said, Sisse Ditlev, Asger Sverrild, Celeste Porsbjerg, Lena Uller, Therese Lapperre","doi":"10.1183/13993003.02441-2025","DOIUrl":"10.1183/13993003.02441-2025","url":null,"abstract":"<p><strong>Background: </strong>Viral respiratory infections are the leading trigger of asthma exacerbations, and impaired epithelial type I and III interferon (IFN) responses may contribute to more severe exacerbations. Azithromycin reduces exacerbations clinically, but its effects on epithelial antiviral immunity remain unclear. This study investigated whether azithromycin treatment enhances airway epithelial antiviral responses and modulates alarmin concentrations in patients with uncontrolled asthma.</p><p><strong>Methods: </strong>In the investigator-initiated, double-blind, placebo-controlled AZIMUNE trial, 40 adults with uncontrolled asthma were randomised (1:1) to azithromycin (500 mg three times per week) or placebo (identical regimen) for 12 weeks. Bronchial epithelial cells were obtained <i>via</i> bronchoscopy at baseline and after week 12, and cultured and infected <i>ex vivo</i> with rhinovirus. Protein levels of IFN-β, IFN-λ, alarmins (interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP)) and pro-inflammatory cytokines were quantified.</p><p><strong>Results: </strong>Azithromycin significantly increased rhinovirus-induced concentrations of IFN-β (p=0.047) and IFN-λ (p=0.013) in the azithromycin group (n=16) compared with baseline, whereas no change was seen in the placebo group (n=16). Azithromycin treatment also reduced IL-33 concentrations (p=0.001), while TSLP levels were unaffected. Clinical outcomes improved numerically in the azithromycin group, but differences <i>versus</i> placebo were not statistically significant.</p><p><strong>Conclusions: </strong>Azithromycin enhances epithelial antiviral immunity and attenuates IL-33 concentrations in response to rhinoviral infection in asthma. The dual immunomodulatory effect of azithromycin supports its role as adjunctive therapy to prevent virus-induced exacerbations.</p>","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13519834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NETs in pleural infection: biological signal or clinical tool?","authors":"José M Porcel, Y C Gary Lee","doi":"10.1183/13993003.00815-2026","DOIUrl":"https://doi.org/10.1183/13993003.00815-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung transplantation for ultra-rare diseases: from anecdote to evidence, a collective responsibility.","authors":"Jérôme Le Pavec, Federica Meloni","doi":"10.1183/13993003.00971-2026","DOIUrl":"https://doi.org/10.1183/13993003.00971-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YY1 lactylation mediates epithelial barrier dysfunction during acute lung injury.","authors":"Ning Li, Yi Liu, Minglang Gao, Wuxiong Zhang, Rui Xiong, Yifan Zuo, Xiao Lu, Bangjun Xu, Chunguang Miao, Qing Geng, Songping Xie, Xiaojing Wu, Bohao Liu","doi":"10.1183/13993003.02717-2025","DOIUrl":"https://doi.org/10.1183/13993003.02717-2025","url":null,"abstract":"<p><p>Elevated lactate levels in lung tissue are a distinct hallmark of acute lung injury (ALI), but the biological functions of glycolytic reprogramming and lactate-derived protein modification in damaged alveolar epithelial cells remain poorly elucidated. In the present study, we validated markedly increased lactate abundance in peripheral samples and lung tissues of multiple ARDS patients and multiple ALI mouse models. Administration of glycolysis inhibitor 2-DG to deplete endogenous lactate effectively mitigated lung injury and alveolar epithelial barrier dysfunction, whereas exogenous lactate supplementation significantly worsened these pathological manifestations. Genetic silencing of pulmonary LDHA <i>via</i> intratracheal injection of AAV9-shLdha successfully reproduced the protective phenotypes conferred by 2-DG treatment. Mechanistically, accumulated lactate facilitated Tip60-dependent lactylation modification of YY1 at lysine 183. Biochemical assays confirmed that YY1 K183 lactylation inhibited the expression of PGC-1α at transcriptional level, further causing mitochondrial homeostasis disorder and destruction of alveolar epithelial barrier. In vivo rescue experiments using lactylation-deficient YY1-K183R mutant verified the essential pathogenic role of this site-specific lactylation in LPS-triggered ALI progression. Additionally, we established two feasible translational therapeutic strategies, including K183-targeted cell-penetrating peptide and glycyrrhizin screened from compound libraries. Both candidates efficiently suppressed YY1 K183 lactylation, restored PGC-1α expression and mitochondrial function, and relieved pulmonary edema, inflammatory infiltration and cell apoptosis. In summary, lactate-driven YY1 K183 lactylation disrupts PGC-1α-mediated mitochondrial quality control and epithelial barrier stability. Intervening this lactate-YY1 lactylation axis provides a reliable and promising therapeutic direction for clinical treatment of ALI and ARDS.</p>","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>ERJ</i> Podcast July 2026: Nerandomilast in progressive pulmonary fibrosis.","authors":"","doi":"10.1183/13993003.E6801-2026","DOIUrl":"https://doi.org/10.1183/13993003.E6801-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 1","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to: The use of spirometry to define airflow obstruction and diagnose COPD.","authors":"David M G Halpin, Sanja Stanojevic","doi":"10.1183/13993003.01241-2026","DOIUrl":"https://doi.org/10.1183/13993003.01241-2026","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"68 2","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A phase 2a, double-blind, randomised, placebo-controlled trial of the myeloperoxidase inhibitor, mitiperstat, in participants with chronic obstructive pulmonary disease.","authors":"Dinesh Saralaya, M Nubli Mustapa, João Ferreira, Janwillem W H Kocks, Wayne Brailsford, Sanna Rosengren, Enti Spata, Maria G Belvisi, Jacob Leander, Camille Riff, Giovanna De Palo, Daniel Windgassen, James D Chalmers, Richard E K Russell, John R Hurst, Adam Śmiałowski, Rod Hughes","doi":"10.1183/13993003.02567-2025","DOIUrl":"https://doi.org/10.1183/13993003.02567-2025","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 <i>versus</i> 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 <i>versus</i> 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.</p><p><strong>Conclusion: </strong>These results indicate that the risks outweigh the benefits of mitiperstat as a treatment for COPD.</p>","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":23.8,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}