European Respiratory Review最新文献

{"title":"Change in pulmonary artery pressure upon acute exposure to high altitude: a systematic review and meta-analysis.","authors":"Eva Cafuta Wagner, Julian Müller, Michael Furian, Dinah Hertig, Alessandro Vella, Daniel Teixeira, Mona Lichtblau, Silvia Ulrich","doi":"10.1183/16000617.0069-2026","DOIUrl":"10.1183/16000617.0069-2026","url":null,"abstract":"<p><strong>Background/research question: </strong>We investigated the increase in pulmonary artery pressure (PAP) with altitude gain in healthy low-altitude residents travelling to high altitude, analysing reported measures including systolic (sPAP) and mean pulmonary artery pressure (mPAP) and tricuspid regurgitation pressure gradient (TRPG).</p><p><strong>Methods: </strong>A systematic literature search was performed in PubMed and Embase from database inception to 12 December 2024. Studies including healthy adults residing at <1000 m and reporting sPAP, mPAP or TRPG measured by echocardiography or right heart catheterisation at both low altitude and >1000 m within 30 days were included. Random effects meta-analyses and meta-regression assessed the increase in sPAP, mPAP and TRPG per 1000 m altitude gain.</p><p><strong>Results: </strong>60 articles with 1220 participants (75% males, age 34±4 years) were eligible; 54 were included into the meta-analysis. sPAP was reported in 38 studies, mPAP in nine and TRPG in 11. At high altitude, absolute sPAP ranged from 24 to 50 mmHg and mPAP from 20 to 26 mmHg. Meta-regression showed a linear increase per 1000 m: sPAP 3.4±0.5 mmHg, mPAP 2.5±0.7 mmHg and TRPG 3.3±1.0 mmHg. The estimated upper limit of normal for the increase per 1000 m was 4.5 mmHg for all three measures.</p><p><strong>Interpretation: </strong>This systematic review and meta-analysis of healthy low-altitude residents travelling to high altitudes demonstrates a linear increase in PAP with altitude gain, based predominantly on data from elevations >2500 m and younger male populations. It defines upper reference limits for the increase in sPAP, mPAP and TRPG per 1000 m. These population-derived reference ranges may assist in the interpretation of PAP measurements and in counselling individuals evaluated at high altitude, but should be applied with consideration of the underlying population and exposure characteristics.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561247","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":"Selective phosphodiesterase 4B inhibition in fibrotic lung disease: a scoping review of vascular-immune mechanisms and extrapulmonary implications.","authors":"Fabio Perrotta, Domenica Francesca Mariniello, Raffaella Pagliaro, Andrea Bianco","doi":"10.1183/16000617.0095-2026","DOIUrl":"10.1183/16000617.0095-2026","url":null,"abstract":"<p><strong>Background: </strong>Preferential phosphodiesterase 4B (PDE4B) inhibition with nerandomilast has demonstrated attenuation of forced vital capacity decline in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis. Because PDE4 enzymes regulate cAMP-dependent inflammatory and endothelial signalling, class-level PDE4 inhibition has been consistently linked to vascular-immune pathways. Whether preferential PDE4B inhibition reproduces these effects remains uncertain.</p><p><strong>Objectives: </strong>To map the available mechanistic and translational literature on extrapulmonary or systemic biological effects of PDE4/PDE4B inhibition and to place nerandomilast trial findings within that framework without inferring clinical efficacy outside pre-specified trial outcomes.</p><p><strong>Methods: </strong>We performed a the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews informed scoping review of PubMed/MEDLINE from database inception to 1 March 2026. Eligible studies included pre-clinical, translational and clinical reports addressing endothelial, immune, microvascular or organ-level effects of PDE4/PDE4B modulation. Evidence was charted and narratively synthesised rather than quantitatively pooled.</p><p><strong>Results: </strong>71 studies were included. Experimental data (primarily derived from class-level PDE4 inhibition) consistently link these pathways to modulation of endothelial permeability, leukocyte-endothelial adhesion, thromboinflammatory signalling, and macrophage resolution programmes across pulmonary and extrapulmonary models. However, most extrapulmonary evidence derives from class-level PDE4 biology rather than nerandomilast-specific investigations, and clinical evidence for extrapulmonary benefit in fibrotic lung disease remains indirect.</p><p><strong>Conclusions: </strong>Because PDE4 enzymes regulate cAMP-dependent inflammatory and endothelial signalling, class-level PDE4 inhibition has been consistently linked to modulation of vascular-immune pathways. Whether preferential PDE4B inhibition reproduces these effects in humans remains to be established. While at present, extrapulmonary clinical benefit in fibrotic lung disease remains unproven, future studies should prospectively evaluate systemic biomarkers and organ-level outcomes rather than relying on <i>post hoc</i> interpretation of numerical signals.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561230","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":"The triple-hit hypothesis: exploring pulmonary e-cigarette, PM_2.5 and viral polyexposure.","authors":"Hilma Clemén, Sangeetha Ramu, Lena Uller","doi":"10.1183/16000617.0036-2026","DOIUrl":"10.1183/16000617.0036-2026","url":null,"abstract":"<p><p>Exposure to e-cigarette aerosols, particulate matter with aerodynamic diameter ≤2.5 µm (PM_2.5) and respiratory viruses rarely occurs in isolation, but rather in complex polyexposure contexts during daily life. On a cellular and molecular level, vaping induces a distinct lipid-laden macrophage phenotype, alters pulmonary neutrophilic infiltration and impairs epithelial differentiation and ciliary function. In contrast, PM_2.5 alters the macrophage polarisation equilibrium, temporally favouring an acute pro-inflammatory phenotype and a subsequent chronic tissue-remodelling phenotype, while also driving an oxidative inflammatory epithelial milieu. Both exposures thus impair antiviral defences and enhance susceptibility to respiratory viral infections such as influenza A, rhinovirus and severe acute respiratory syndrome coronavirus 2. The triple-hit hypothesis proposes that concurrent exposure to vaping aerosols, PM_2.5 and respiratory viruses may exert additive or synergistic effects on chronic airway inflammation. PM_2.5 may amplify vaping-induced macrophage lipid accumulation, thereby reducing the macrophage clearance capacity. Decreased efferocytosis and autophagy may further exacerbate inflammation by increasing secondary necrosis from apoptotic cells and debris. This persistent inflammatory state coupled with epithelial injury and impaired antiviral responses may increase the risk of infection and accelerate the development or progression of chronic respiratory diseases such as asthma and COPD. These insights highlight the crucial need for polyexposure models to accurately reflect real-world environmental and behavioural exposures and evaluate their impact on respiratory health and disease exacerbations. Understanding this exposure triad is also crucial for refining exposure guidelines, updating risk assessments and implementing preventive strategies.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561264","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":"Beyond nocturnal hypercapnia: positioning obstructive sleep apnoea within a sleep-circadian-hypothalamic network.","authors":"Yu-Hsiang Lin, Kuo-Jen Lin, Jau-Yuan Chen","doi":"10.1183/16000617.0185-2026","DOIUrl":"10.1183/16000617.0185-2026","url":null,"abstract":"","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561288","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":"Early-life respiratory syncytial virus infection and asthma.","authors":"Jessica Tolentino, Madison Coward-Smith, Brian G G Oliver, Richard Y Kim, Chantal Donovan","doi":"10.1183/16000617.0284-2025","DOIUrl":"10.1183/16000617.0284-2025","url":null,"abstract":"<p><p>Respiratory infections during critical periods of lung development can shape immune responses and cause lasting alterations in pulmonary structure and function. Lung development begins <i>in utero</i>, with airway branching, alveolarisation and epithelial differentiation continuing postnatally, making the lungs particularly vulnerable to early-life insults. Early-life respiratory syncytial virus infections are a major cause of severe respiratory diseases. Furthermore, risks are amplified by preterm birth and specific maternal environmental exposures. In this review, we discuss how early-life respiratory syncytial virus infection can disrupt normal lung development, predisposing to recurrent wheeze, asthma and other chronic lung diseases. We also discuss mechanistic studies, demonstrating how pathogenesis involves a complex interplay between epigenetic regulation, immune activation and airway remodelling. Finally, we highlight preclinical models that have provided some mechanistic insights into the determinants of lung health outcomes and the urgent need for better translational models to gain a deeper understanding of these processes. The intent of this review is to create impetus for developing targeted preventative and therapeutic strategies to mitigate the long-term impact of early-life viral infections on respiratory health.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561292","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":"Comparative response to pharmacological management of asthma in overweight/obese children <i>versus</i> their counterparts: a systematic review and call for data.","authors":"Jose A Castro-Rodriguez, Samantha H Averill, M Isabel Castro-Guevara, Francine M Ducharme","doi":"10.1183/16000617.0311-2025","DOIUrl":"10.1183/16000617.0311-2025","url":null,"abstract":"<p><strong>Background: </strong>Obese children with asthma experience higher morbidity than their counterparts; whether different treatments should be considered remains to be clarified.</p><p><strong>Objective: </strong>To explore the potential group differences in the treatment response to any asthma medications between overweight/obese and normal/underweight children.</p><p><strong>Methods: </strong>We systematically reviewed case-control, cohort studies and randomised controlled trials (RCTs) examining treatment effects by weight status, identified in four bibliographic databases from inception until January 2025. A narrative synthesis was presented because a meta-analysis could not be conducted due to methodological issues.</p><p><strong>Results: </strong>Nine studies (one RCT, five <i>post hoc</i> analyses of RCTs, two cohorts, and one <i>post hoc</i> analysis of a case-control study), including 7089 children (33.9% overweight/obese), met the inclusion criteria. Pharmacological treatment pertained to step 1-2 (n=1), step 2 (n=3), step 3 (n=2), step 5 (n=2), and bronchodilator-response (n=1). Compared with normal weight, step 1-2 showed a trend toward reduced inhaled corticosteroid (ICS) efficiency in minimising symptom days in overweight/obese preschoolers. Regarding step 2 monotherapy, overweight/obese children may benefit as much (or more) from nedocromil or leukotriene receptor antagonist (LTRA) than from ICS. In step 3, adding LTRA (<i>versus</i> placebo) to ICS monotherapy was more effective, whereas higher-dose ICS monotherapy was less effective than LTRA or long-acting β₂-agonist (LABA) combination therapy in obese than normal-weight children; adding LABA appears equally effective across weight groups. A similar or better response to omalizumab was observed in obese compared to nonobese children.</p><p><strong>Conclusion: </strong>While no firm recommendations could be made regarding potential differential treatment responses, the superiority of ICS monotherapy or step-up therapy compared to other controllers appears lost in overweight/obese children.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561323","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":"Genetic susceptibility to respiratory health effects from outdoor air pollution: a structured narrative review.","authors":"Yidan Meng, Ji Soo Lim, Christine Chen, Christopher F Rider, Min Hyung Ryu, Christopher Carlsten","doi":"10.1183/16000617.0326-2025","DOIUrl":"10.1183/16000617.0326-2025","url":null,"abstract":"<p><p>Outdoor air pollution exposure is a well-established driver of respiratory disease, while growing evidence highlights an important role for genetic susceptibility. Building on this expanding body of work, our review synthesises findings across studies and provides an integrated overview. Here, we present a structured literature review summarising study characteristics and statistically significant single nucleotide polymorphisms (SNPs) reported in gene-environment interaction studies of air pollution related respiratory outcomes. By consolidating this evidence, the review clarifies current findings and supports more rigorous, evidence-based risk stratification in future observational and intervention studies. We included 48 peer-reviewed studies in humans published between 2014 and 2024 that examined gene-environment interactions involving SNPs, outdoor air pollution exposure and respiratory outcomes. Studies primarily evaluating particulate matter with aerodynamic diameter <2.5 µm and <10 μm, and nitrogen dioxide included respiratory end-points, such as asthma, COPD and lung-function measures. The majority of analyses used regression-based methods, supplemented by mixed-effects and generalised estimating equation models. Candidate gene studies (particularly in the glutathione S-transferase (GST) family) along with polygenic risk scores and genome-wide interaction approaches identified 89 SNPs across 53 genes. Replicated variants involved pathways in oxidative stress detoxification (<i>e.g.</i> rs1695 (<i>GSTP1</i>) and rs2266637 (<i>GSTT1</i>)) and inflammatory responses (<i>e.g.</i> rs1800629 (<i>TNF</i>), rs3804099 (<i>TLR2</i>) and rs848 (<i>IL13</i>)), consistently modifying pollution-related lung function decline and airway inflammation. By consolidating key genes, study designs and analytic methods, this review provides a curated SNP list to inform future genetic risk stratification. We highlight the need for studies in ancestrally diverse populations, controlled human exposure designs, and multi-omics approaches to strengthen mechanistic understanding of gene-environment interactions in respiratory health.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411141","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":"Risk prediction for lung cancer screening: a systematic review and meta-regression.","authors":"Ramin Rezaeianzadeh, Crystal Leung, Soo Jeong Kim, Kayly Choy, Kate M Johnson, Miranda Kirby, Stephen Lam, Benjamin M Smith, Mohsen Sadatsafavi","doi":"10.1183/16000617.0295-2025","DOIUrl":"10.1183/16000617.0295-2025","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer (LC) remains the deadliest cancer, often diagnosed at advanced stages. Screening reduces mortality in high-risk individuals. Eligibility criteria in European and US screening guidelines have recently expanded. Therefore, we conducted an updated systematic review of risk-based models for identifying candidates for low-dose computed tomography screening and post-screening nodule classification.</p><p><strong>Methods: </strong>We systematically searched Embase and Medline (January 2020-January 2026), identifying studies proposing new risk models in the context of LC screening. We separated models by pre- and post-screening risk stratification. Data extraction included study design, population, model type, risk horizon and model performance metrics. We performed an exploratory meta-regression of areas under the curve (AUCs) to assess whether sample size, model type, validation type and inclusion of biomarkers were associated with performance.</p><p><strong>Results: </strong>Of 2462 records, 91 were included. 56 models were for screening selection (30 included biomarkers) and 35 for post-screening nodule classification. Regression-based models predominated, though machine-learning approaches were increasingly common. Discrimination ranged from moderate (AUC∼0.70) to excellent (>0.90), with biomarker and imaging-enhanced models often outperforming models without. Calibration was inconsistently reported and fewer than half underwent external validation.</p><p><strong>Conclusion: </strong>We identified 91 risk prediction models for LC, developed after 2020. Although many demonstrated promising discrimination across both screening selection and post-screening management, most remain insufficiently mature for clinical adoption, as their performance and practical value outside the original study setting are uncertain. Future work should prioritise external validation, updating and comparative evaluation of existing models, and prospective implementation studies rather than continued development of additional models.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411138","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":"Prediction of PD-L1 expression in nonsmall cell lung cancer using artificial intelligence models based on radiomics: a systematic review and meta-analysis.","authors":"Peng Zhang, Biao Zhang, Nian Liu, Delong Huang, Haoshu Zhong, Junhao Wu, Yiren Wang, Qiang Ren","doi":"10.1183/16000617.0299-2025","DOIUrl":"10.1183/16000617.0299-2025","url":null,"abstract":"<p><strong>Background: </strong>Since 1992, the incidence of lung cancer has shown an overall downward trend, with survival rates significantly improving in recent years due to the application of immune checkpoint inhibitors (ICIs). Assessing programmed death ligand 1 (PD-L1) expression status in lung cancer patients is crucial for predicting the efficacy of ICIs and formulating treatment plans. Therefore, there is an urgent need to assess PD-L1 expression status in lung cancer patients, particularly those with nonsmall cell lung cancer (NSCLC). While numerous studies have demonstrated promising results using artificial intelligence (AI) models based on radiomics, current understanding in this area remains incomplete.</p><p><strong>Method: </strong>We conducted a search of medical databases and screened studies that meet the criteria. We performed feature extraction and data extraction from these studies, analysed them using R software, and generated forest plots. We conducted subgroup analyses based on imaging modality and algorithm model.</p><p><strong>Results: </strong>A total of 35 studies were included in the analysis. For the Tumor Proportion Score (TPS)1 group, the pooled area under the curve (AUC) for the validation set was 0.782. For the TPS50 group, the pooled AUC for the validation set was 0.798. Subgroup analysis revealed that machine learning performed better when predicting TPS50, while deep learning was superior for predicting TPS1. When predicting TPS, prediction models constructed using 2<i>-</i>fluoro-2-deoxy-d-glucose (¹⁸F) positron emission tomography/computed tomography (CT) and contrast-enhanced CT outperformed those based on noncontrast CT. Conversely, when predicting a TPS, the noncontrast-CT-based prediction model significantly outperformed the other two groups.</p><p><strong>Conclusions: </strong>Imaging modality and algorithm model are key factors influencing AI prediction models for PD-L1 expression in NSCLC patients.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411115","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":"Fibrotic chronic eosinophilic pneumonia: from inflammation to fibrosis and therapeutic implications.","authors":"Daniele Previtero, Gioele Castelli, Ylenia Padrin, Francesca Scalvenzi, Isabella Ruzzon, Elisabetta Cocconcelli, Mariaenrica Tinè, Elisabetta Balestro, Roberto Padoan, Marco Caminati, Simonetta Baraldo, Paolo Spagnolo, Umberto Semenzato","doi":"10.1183/16000617.0076-2026","DOIUrl":"10.1183/16000617.0076-2026","url":null,"abstract":"<p><p>Chronic eosinophilic pneumonia is a rare inflammatory lung disease that typically responds to systemic glucocorticoids but is frequently complicated by relapses and treatment-related toxicity. In recent years, monoclonal antibodies targeting the interleukin-5 (IL-5) pathway have emerged as effective glucocorticoid-sparing therapies in relapsing or glucocorticoid-dependent chronic eosinophilic pneumonia. Alongside these advances, a substantial proportion of patients develops progressive fibrotic changes over time, challenging the traditional view of chronic eosinophilic pneumonia as a fully reversible condition. This narrative review summarises current clinical evidence on the use of anti-IL-5/IL-5 receptor subunit α biologicals in chronic eosinophilic pneumonia, examines the emerging phenotype of fibrotic chronic eosinophilic pneumonia, and discusses the mechanistic links between eosinophilic inflammation and pulmonary fibrosis. We also review experimental and clinical data implicating eosinophils, type 2 cytokines, epithelial alarmins and extracellular traps in fibroblast activation and extracellular matrix deposition, providing a biological rationale for a continuum from inflammation to irreversible lung remodelling. Available data on the use of IL-5-targeted therapies in fibrotic disease are limited, and no prospective studies have specifically addressed this patient population. Conversely, antifibrotic agents such as nintedanib have demonstrated efficacy in progressive fibrosing interstitial lung diseases but have been rarely studied in eosinophilic lung disorders. We propose a phenotype-adapted therapeutic framework in which sustained control of eosinophilic inflammation aims to prevent fibrotic progression in early disease, while antifibrotic therapy may be considered in patients with established or progressive fibrosis. Fibrotic chronic eosinophilic pneumonia thus represents a clinical entity at the crossroads between inflammation and fibrosis, requiring individualised management strategies and dedicated future studies.</p>","PeriodicalId":12166,"journal":{"name":"European Respiratory Review","volume":"35 181","pages":""},"PeriodicalIF":10.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411118","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}