Respiratory Research最新文献

{"title":"Second hand smoke attributable disease burden in 204 countries and territories, 1990-2021: a systematic analysis from the Global Burden of Disease Study 2021.","authors":"Zheng Su, Ying Xie, Zhenxiao Huang, Anqi Cheng, Xinmei Zhou, Min Wang, Xin Xia, Tingfen Ji, Liang Zhao, Zhao Liu, Dan Xiao, Chen Wang","doi":"10.1186/s12931-025-03228-3","DOIUrl":"https://doi.org/10.1186/s12931-025-03228-3","url":null,"abstract":"<p><strong>Background: </strong>We aimed to estimate the changes in, second hand smoke (SHS) and potential drivers of its health outcome from 1990 to 2021 worldwide.</p><p><strong>Methods: </strong>The data was derived from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021, which covered 204 countries and territories. We reported SHS changes by sex, year and sociodemographic index (SDI) level (a summary measure that identifies where countries or other geographic areas sit on the spectrum of development) from 1990 to 2021. We analyzed the risk-outcome pairs among all age groups to estimate disease burden attributable to SHS exposure and also did a decomposition method to attribute changes in all-cause SHS attributable deaths or disability-adjusted life years (DALYs) to population growth, population aging, and mortality change.</p><p><strong>Results: </strong>Worldwide, the age-standardized summary exposure values (SEV) of SHS exposure in 2021 was 30.6% (28.9 to 31.6) for males and 38.0% (35.5 to 39.0) for females, with a percentage change of -0.2 (-0.2 to -0.1) and -0.3 (-0.3 to -0.2), respectively, since 1990. Among the top 10 countries with the highest SEV, there were mainly high-middle SDI countries for male and low-middle SDI and middle SDI countries for female, respectively. Secondly, about 1.29 million deaths (0.68-1.90) and 34.90 million DALYs (17.95-52.21) were attributable to SHS exposure, and about half of them took place in two countries (China and India). Ischemic heart disease (IHD) (29.67%), chronic obstructive pulmonary disease (COPD) (19.04%), and lower respiratory infections (LRIs) (10.87%) were the three leading causes of SHS associated deaths. Lastly, since 2010, the number of SHS related death significantly increased due to population growth and population aging, despite a decrease in mortality attributable to SHS exposure.</p><p><strong>Conclusion: </strong>Globally, the age-standardized SEV of SHS exposure decreased from 1990 to 2021. Since 2010, the increased number of deaths attributable to SHS exposure was mainly attributable to population growth and aging.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"174"},"PeriodicalIF":5.8,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exhaled volatile organic compounds as novel biomarkers for early detection of COPD, asthma, and PRISm: a cross-sectional study.","authors":"Jiaxin Tian, Qiurui Zhang, Minhua Peng, Leixin Guo, Qianqian Zhao, Wei Lin, Sitong Chen, Xuefei Liu, Simin Xie, Wenxin Wu, Yijie Li, Junqi Wang, Jin Cao, Ping Wang, Min Zhou","doi":"10.1186/s12931-025-03242-5","DOIUrl":"https://doi.org/10.1186/s12931-025-03242-5","url":null,"abstract":"<p><strong>Background: </strong>Globally, chronic respiratory diseases have become the third leading cause of death, including chronic obstructive pulmonary disease (COPD) and asthma, and have been threatening human life for a long time. To alleviate the disease burden, it is crucial to develop rapid and convenient screening methods for COPD, preserved ratio impaired spirometry (PRISm), and asthma. Volatile organic compounds (VOCs) in breath can reflect the pathophysiological processes of disease, thereby having the potential to serve as a promising approach for diagnosing respiratory diseases. Can we identify VOC markers in breath with the potential to serve as classification indicators, and further establish learning models for the early detection of COPD, asthma, or PRISm patients?</p><p><strong>Methods: </strong>This is a cross-sectional study in which exhaled breath samples were collected from 184 patients with COPD, 66 patients with asthma, 72 PRISm individuals, and 45 healthy individuals. From August 2023 to June 2024, the breath samples were analyzed using portable micro gas chromatography (CXBA-Alpha, ChromX Health Co., Ltd.). Potential VOC markers for classification were identified by univariate and multivariate analyses. Subsequently, classification models were established by machine learning algorithms, based on these VOC markers along with baseline characteristics. The sensitivity, specificity, and accuracy of these models were calculated to assess their overall discriminatory performance.</p><p><strong>Results: </strong>A total of 367 patients were enrolled in our study. We identified nine VOCs distinguishing COPD patients from healthy controls, nine VOCs differentiating the PRISm population from healthy controls, five VOCs separating asthma patients from healthy controls, five VOCs distinguishing COPD patients from asthma patients, and seven VOCs differentiating the PRISm population from asthma patients based on breathomics feature selection. We utilized five algorithms to establish diagnostic models and selected the optimal one among them. The random forest model best distinguished COPD from healthy controls with an area under the receiver operating characteristic curve (AUC) of 0.92 ± 0.01. The support vector classifier (SVC) model was most effective in separating PRISm from healthy controls, achieving an AUC of 0.78 ± 0.01. Logistic regression performed well in discriminating asthma from PRISm (AUC, 0.74 ± 0.02) and COPD (AUC, 0.92 ± 0.01), in contrast, the random forest model differentiated asthma from healthy controls with an AUC of 0.81 ± 0.02.</p><p><strong>Conclusion: </strong>VOC panel-based classification models have the potential to be a novel strategy for the discrimination of chronic respiratory diseases. Using the portal micro gas chromatography enables swift detection of chronic respiratory disease and, most importantly, facilitates the rapid identification of PRISm individuals within the population.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"173"},"PeriodicalIF":5.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of periodontal therapy on lung function: a twelve-month follow-up intervention study.","authors":"Anders Røsland, Randi J Bertelsen, Joachim Heinrich, Stein Atle Lie, Andrei Malinovschi, Dagmar F Bunæs","doi":"10.1186/s12931-025-03246-1","DOIUrl":"https://doi.org/10.1186/s12931-025-03246-1","url":null,"abstract":"<p><strong>Background: </strong>Evidence suggest an inflammatory link between respiratory health and periodontitis. This study aims to evaluate the impact of periodontal therapy on lung function.</p><p><strong>Methods: </strong>Sixty-two never-smoking patients with mild periodontitis and without other medical conditions participated in this single-blind, prospective trial. Patients underwent periodontal therapy following an infection control approach. Lung function was measured using forced oscillation technique, assessing airway resistance and reactance, and spirometry evaluating FEV₁, FVC, and FEV₁/FVC. Lung function and fractional exhaled nitric oxide were assessed at baseline, three and six weeks, and every three months for a year. Periodontal parameters were recorded at baseline, six weeks, six and 12 months. Data were analysed using mixed-effects regression models.</p><p><strong>Results: </strong>Patients (mean age 36 years, 58% female) showed significant improvements in periodontal parameters (p < 0.001). Oscillometry revealed a significant decrease in airway resistance at 11 Hz and 19 Hz after six weeks, with further significant decreases throughout the study. Resistance at 5 Hz (R₅) consistently declined, reaching significance at three months (p = 0.001). By one year, R₅, R₁₁, R₁₉, and R_5 - 20 showed significant reductions (all p < 0.05). Airway reactance at 5 Hz became less negative at three months (p = 0.002), while the reactance area (AX) decreased significantly at six months (p = 0.008). No significant changes were observed in spirometry or fractional exhaled nitric oxide.</p><p><strong>Conclusion: </strong>A decrease in airway resistance was observed after periodontal therapy, underscoring its positive impact on small airway function. These findings suggest that oral infection control is valuable for respiratory health in young adults before chronic conditions establish.</p><p><strong>Clinical trial registration: </strong>The trial was registered at ClinicalTrials.gov (NCT04781153) on February 19, 2021, prior to participant enrolment.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"172"},"PeriodicalIF":5.8,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purpose in life and lung function: an individual-participant meta-analysis of six cohort studies.","authors":"Angelina R Sutin, Yannick Stephan, Martina Luchetti, Justin Brown, Tiia Kekäläinen, André Hajek, Brice Canada, Sébastien Kuss, Antonio Terracciano","doi":"10.1186/s12931-025-03247-0","DOIUrl":"https://doi.org/10.1186/s12931-025-03247-0","url":null,"abstract":"<p><strong>Background: </strong>Purpose in life is a psychological resource associated with better health outcomes across adulthood. It is unknown whether it is related to lung function, a key marker of health and longevity. We evaluate the replicability and generalizability of the cross-sectional association between purpose in life and lung function and whether purpose in life is associated with lower risk of developing poor lung function over time.</p><p><strong>Methods: </strong>Participants were from six cohort studies with public data: Health and Retirement Study, Midlife in the United States study, Wisconsin Longitudinal Study, National Health and Aging Trends Study, English Longitudinal Study of Ageing, and Survey of Health, Ageing and Retirement in Europe (total N = 85,190). Participants reported on their purpose in life, and staff measured their peak expiratory flow with either a peak flow meter or a spirometer. Four cohorts (N = 11,595) had longitudinal assessments of lung function over up to 12 years. Linear regression was used to test the cross-sectional association between purpose and continuous lung function. Cox regression was used to test the association between purpose and risk of developing predicted lung function < 80% over time, a dichotomous outcome that categorized lung function into performance less than 80% of predicted function (= 1) and at least 80% of predicted function (= 0).</p><p><strong>Results: </strong>In each cohort and aggregated in a random-effects meta-analysis, higher purpose in life was associated with better peak expiratory flow (meta-analytic effect = 0.07, p <.001). The association was generally similar across sociodemographic groups (e.g., age, sex). Every standard deviation higher purpose in life was associated with a 10% reduced risk of developing poor lung function over time (meta-analytic hazard ratio = 0.91, 95% confidence interval = 0.88, 0.94, p <.001). These associations were attenuated but remained significant accounting for behavioral and clinical risk factors.</p><p><strong>Conclusions: </strong>Purpose in life is associated with healthier lung function, with evidence of replicability and generalizability, and with lower risk of developing poor lung function over time. Lung function may be one mechanism between purpose in life and healthier outcomes in older adulthood.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"171"},"PeriodicalIF":5.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based Diagnostic model for determining the etiology of pleural effusion using Age, ADA and LDH.","authors":"Qing-Yu Chen, Shu-Min Yin, Ming-Ming Shao, Feng-Shuang Yi, Huan-Zhong Shi","doi":"10.1186/s12931-025-03253-2","DOIUrl":"https://doi.org/10.1186/s12931-025-03253-2","url":null,"abstract":"<p><strong>Background: </strong>Classification of the etiologies of pleural effusion is a critical challenge in clinical practice. Traditional diagnostic methods rely on a simple cut-off method based on the laboratory tests. However, machine learning (ML) offers a novel approach based on artificial intelligence to improving diagnostic accuracy and capture the non-linear relationships.</p><p><strong>Method: </strong>A retrospective study was conducted using data from patients diagnosed with pleural effusion. The dataset was divided into training and test set with a ratio of 7:3 with 6 machine learning algorithms implemented to diagnosis pleural effusion. Model performances were assessed by accuracy, precision, recall, F1 scores and area under the receiver operating characteristic curve (AUC). Feature importance and average prediction of age, Adenosine (ADA) and Lactate dehydrogenase (LDH) was analyzed. Decision tree was visualized.</p><p><strong>Results: </strong>A total of 742 patients were included (training cohort: 522, test cohort: 220), 397 (53.3%) diagnosed with malignant pleural effusion (MPE) and 253 (34.1%) with tuberculous pleural effusion (TPE) in the cohort. All of the 6 models performed well in the diagnosis of MPE, TPE and transudates. Extreme Gradient Boosting and Random Forest performed better in the diagnosis of the MPE, with F1 scores above 0.890, while K-Nearest Neighbors and Tabular Transformer performed better in the diagnosis of the TPE, with F1 scores above 0.870. ADA was identified as the most important feature. The ROC of machine learning model outperformed those of conventional diagnostic thresholds.</p><p><strong>Conclusions: </strong>This study demonstrates that ML models using age, ADA, and LDH can effectively classify the etiologies of pleural effusion, suggesting that ML-based approaches may enhance diagnostic decision-making.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"170"},"PeriodicalIF":5.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12048966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics characterization of early chronic obstructive pulmonary disease.","authors":"Bolun Li, Jiangfeng Liu, Yinghao Cao, Yiyang Wang, Sinan Wu, Huiyuan Hu, Xingqi Xiao, Jiantao Hu, Qian Wang, Junlin Wu, Le Luo, Yong Liu, Qihao Tang, Yanjiang Xing, Tiantian Zhang, Jinyu Zhou, Lin Wang, Juntao Yang, Jing Wang, Chen Wang","doi":"10.1186/s12931-025-03250-5","DOIUrl":"https://doi.org/10.1186/s12931-025-03250-5","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is projected to become the third leading cause of death globally by 2030, accounting for 71.9% of chronic respiratory diseases cases in 2019. Early COPD (ECOPD) diagnosis heavily relies on clinically monitoring of lung functions, with a strong influence from smoking exposures, which may not align well with disease progression. As such, the GOLD 2022-2024 guidelines emphasize the discovery of biological markers over clinical symptoms for early detection. This study explores the biological characteristics of ECOPD in a cohort of 176 adults from China Pulmonary Health Study, consisting 88 healthy controls (HC) and 88 clinically diagnosed ECOPD, matched for age, gender and smoking history. While lung function tests revealed differences between HC and ECOPD, no significant distinctions were observed in routine blood tests. Proteomics analysis identified 377 plasma proteins common to both groups, with low-intensity proteins driving group-specific differences. Univariable logistic regression and gene set enrichment analysis identified 248 proteins associated with ECOPD, particularly those involved in inflammation process. Validation in an independent cohort confirmed the association of 15 proteins with ECOPD. Metabolomics analysis of the plasma identified 1788 metabolites, 137 of which were found linked to ECOPD. Machine learning models indicated that a multi-omics approach provided the best predication of lung function (R² = 0.74), while proteomics alone effectively diagnosed ECOPD (AUC = 0.949). Similarity network fusion and clustering revealed two ECOPD subgroups: one by markers of inflammatory-immune response, and the other by the presence of those related to hemostasis or the vascular smooth muscle function. These findings underscore the potential of multi-omics integration in distinguishing ECOPD subgroups and predicting disease risk.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"167"},"PeriodicalIF":5.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12039082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated metabolic pathways of pulmonary fibrosis and the lipids associated with the effects of nintedanib therapy.","authors":"Yasuo Shimizu, Yasuhiro Horibata, Mariko Domae, Yusuke Nakamura, Tatsuya Yokoyama, Ryo Arai, Taichi Shiobara, Akihiro Takemasa, Ryosuke Koike, Nobuhiko Uchida, Meitetsu Masawa, Rinna Tei, Taiji Watanabe, Hiroko Morita, Masaaki Miyoshi, Sayo Soda, Seiji Niho, Ko Igami, Hiroyuki Sugimoto","doi":"10.1186/s12931-025-03239-0","DOIUrl":"https://doi.org/10.1186/s12931-025-03239-0","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary fibrosis (PF) is a disease with a poor prognosis, and its pathogenesis is not fully understood. Identifying dysregulation of lipid metabolism in PF may provide insight and promote the development of novel therapies. The present study was designed to clarify the dysregulated lipid pathways and identify lipids correlated with treatment response.</p><p><strong>Methods: </strong>This research comprised two prospective cohort studies. Study 1 aimed to identify dysregulated metabolic pathways and lipids in the peripheral blood of PF patients, compared with healthy control (HC) subjects. Study 2 aimed to identify lipids associated with the decline in % forced vital capacity (%FVC) and survival in PF patients treated with the anti-fibrotic drug, nintedanib. As a preliminary ancillary experiment, we attempted to identify the lipids associated with endothelial cells and fibroblasts.</p><p><strong>Results: </strong>In Study 1, 38 lipids were identified that differed between the PF (n = 66) and HC (n = 63) groups. Compared with the HC subjects, phosphatidylcholine (PC) 36:5 was the most up-regulated and lysophosphatidylcholine (LPC) 18:0 was the most down-regulated in PF patients. Glycerophospholipid metabolism was the most enriched pathway. Plasmenyl phosphatidylethanolamine (pPE) and plasmanyl phosphatidylcholine (pPC) were determined to be endothelial-related lipids, and phosphatidylethanolamine (PE) were fibroblast-related lipids in PF. In Study 2, 10 lipids were identified that differed between the absolute decline in %FVC < 2.5% group (6 M responders, n = 14) and the decline in %FVC > 2.5% group (6 M non-responders, n = 6) after 6 M of nintedanib therapy, and 6 lipids were identified that differed between the absolute decline in %FVC < 5% group (12 M responders, n = 15) and the decline in %FVC > 5% group (12 M non-responders, n = 5) after 12 M of nintedanib therapy. Four lipids were consistently detected at 6 M and 12 M, and among them, higher levels of pPE 18:0p/22:6 at 6 M showed a poorer prognosis for 24 M survival (p < 0.05, HR = 6.547, 95% CI = 1.471-29.13). Under nintedanib therapy, pPE species were correlated with progressive fibrosis, and pPE 18:0p/22:6 was considered an endothelial-related lipid.</p><p><strong>Conclusions: </strong>Lipidomic profiling revealed distinct pathways in PF patients. pPE species were strongly associated with the responses to nintedanib therapy. Targeting the lipids or catabolic enzymes involved in dysregulated pathways has the potential to ameliorate PF.</p><p><strong>Trial registration: </strong>Registry for UMIN, Lipidomic analysis on plasma in idiopathic pulmonary fibrosis patients. Trial registry number, UMIN000020872. Registered 3 February 2016, https://center6.umin.ac.jp/cgiopenbin/ctr/index.cgi .</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"166"},"PeriodicalIF":5.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144040111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alveolar cell composition in interstitial lung disease and the development of a pulmonary progressive fibrosing phenotype: a retrospective cohort study.","authors":"Iris A Simons, Bart G Boerrigter, Maud C M Hovestadt, Kirsten A Mooij-Kalverda, Shiqi Zhang, Leonoor S Boers, Anke H Maitland- van der Zee, Esther J Nossent, Jan Willem Duitman","doi":"10.1186/s12931-025-03236-3","DOIUrl":"https://doi.org/10.1186/s12931-025-03236-3","url":null,"abstract":"<p><strong>Background: </strong>Immunological bronchoalveolar lavage (iBAL) is a frequently employed diagnostic tool in interstitial lung disease (ILD). The association between iBAL cellular composition and disease progression remains elusive. We evaluated whether the alveolar cellular composition at initial diagnosis is predictive of the development of progressive pulmonary fibrosis (PPF) in patients with ILD.</p><p><strong>Methods: </strong>A retrospective analysis of 111 patients diagnosed with ILD who underwent iBAL for diagnostic purposes between January 2018 and January 2023 was conducted. The identification of PPF was based on the criteria outlined in the ATS/ERS/JRS/ALAT clinical practice guidelines. Clinical data, pulmonary function tests, radiological imaging, and BAL cellular composition were collected. Groups were compared using the non-parametric Wilcoxon rank sum test. Linear mixed-effect modelling was used to assess the association between baseline cell composition and longitudinal lung function decline.</p><p><strong>Results: </strong>A total of 33.3% of patients exhibited a PPF phenotype. A significant association between baseline iBAL CD4 + and CD8 + T cell percentages and forced vital capacity (FVC) decline within the first year was observed. Other cell types were not associated with ILD progression within one-year of follow-up.</p><p><strong>Conclusions: </strong>CD4 + and CD8 + T cell percentages significantly correlated with FVC changes in patients with fibrotic ILD. No further associations were found between the baseline iBAL cellular profiles and disease progression. These findings suggest that baseline iBAL cellular profiles may hold some promise in predicting fibrotic ILD disease progression. Further (prospective) studies using larger cohorts may be needed to elucidate the association between the cellular composition of iBAL fluid and pulmonary fibrosis progression.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"164"},"PeriodicalIF":5.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung function decline and incidence of chronic obstructive pulmonary disease in participants with spirometry-defined small airway dysfunction: a 15-year prospective cohort study in China.","authors":"Yumin Zhou, Fan Wu, Zhishan Deng, Zihui Wang, Heshen Tian, Peiyu Huang, Youlan Zheng, Huajing Yang, Ningning Zhao, Cuiqiong Dai, Changli Yang, Shuqing Yu, Jia Tian, Jiangyu Cui, Shengming Liu, Dali Wang, Xiaoping Wang, Jiachun Lu, Nanshan Zhong, Pixin Ran","doi":"10.1186/s12931-025-03244-3","DOIUrl":"https://doi.org/10.1186/s12931-025-03244-3","url":null,"abstract":"<p><strong>Background: </strong>Small airway dysfunction (SAD) is common but little is known about the longitudinal prognosis of spirometry-defined SAD. Therefore, we aimed to evaluate the risk of lung function decline and incident chronic obstructive pulmonary disease (COPD) of spirometry-defined SAD.</p><p><strong>Methods: </strong>It was a population-based prospective cohort study conducted in Guangdong, China. Participants were enrolled in the years 2002, 2008, 2012, 2017, and 2019, and those who completed baseline demographic data, a standardized epidemiological questionnaire for COPD, and spirometry were included. Follow-up visits were conducted every three years after enrolment, with a maximum follow-up time of 15 years and a minimum follow-up time of 3 years. Spirometry-defined SAD was defined as having at least two out of three parameters (maximal mid-expiratory flow, forced expiratory flow 50%, and forced expiratory flow 75%) below 65% of the predicted value. Non-obstructive SAD and obstructive SAD were further differentiated based on the presence of airflow obstruction (forced expiratory volume in one second [FEV₁]/forced vital capacity [FVC] < 0.70). Pre- and post-bronchodilator spirometry measurements were analyzed separately.</p><p><strong>Results: </strong>Pre-bronchodilator spirometry dataset included 4680 participants (mean age 55.3 [10.8] years, 2194 [46.9%] males). Participants with pre-bronchodilator SAD had a significantly faster annual decline of FEV₁ % of predicted value (0.31 ± 0.05 vs. 0.20 ± 0.03 %/year; difference: 0.12 [95% confidence interval: 0.01-0.23]; P = 0.023), FVC, and FVC % of predicted value compared to those without pre-bronchodilator SAD. The annual decline of lung function in participants with pre-bronchodilator non-obstructive SAD was not significantly different from that in pre-bronchodilator healthy controls, but they were more likely to progress to spirometry-defined COPD (adjusted hazard ratio: 2.92 [95% confidence interval: 2.28-3.76], P < 0.001). Post-bronchodilator spirometry dataset yielded similar results.</p><p><strong>Conclusions: </strong>Individuals with spirometry-defined SAD have a faster decline in lung function compared to those without SAD, and non-obstructive SAD is more likely to progress to spirometry-defined COPD.</p><p><strong>Trial registration: </strong>Chinese Clinical Trials Registration ChiCTR1900024643. Registered on 19 July 2019.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"169"},"PeriodicalIF":5.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12039187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low levels of DNA repair enzyme NEIL2 May exacerbate inflammation and genomic damage in subjects with stable COPD and during severe exacerbations.","authors":"Victor J Cardenas, Justin B Seashore, Nisha Tapryal, Moe Ameri, Rosalinda Rivera, Kabir Sharma, Tapas Hazra","doi":"10.1186/s12931-025-03251-4","DOIUrl":"https://doi.org/10.1186/s12931-025-03251-4","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory airway disease that is an independent risk factor for lung cancer. Reduction in NEIL2 function, a DNA glycosylase involved in DNA repair during transcription, has been associated with an increased incidence of malignancies in humans. NEIL2 knockout mouse models have demonstrated increased inflammation and oxidative DNA damage in the lungs after exposure to an inflammatory insult, but data are lacking regarding NEIL2 function in individuals with COPD. We investigated whether NEIL2 levels and oxidative DNA damage to the transcribed genome are reduced in individuals with stable COPD and during severe acute exacerbations of COPD (AECOPD).</p><p><strong>Methods: </strong>The study was conducted at a single center in the US. Eligible subjects underwent a one-time 30 cc venous blood draw. The population consisted of 50 adults: 16 with stable COPD, 11 hospitalized for AECOPD, and 23 individuals without lung disease (controls). We analyzed blood leukocytes for NEIL2 mRNA and DNA damage by RT‒qPCR and LA‒qPCR, respectively, in all groups. Plasma levels of seven biomarkers, CXCL1, CXCL8, CXCL9, CXCL10, CCL2, CCL11 and IL-6, were analyzed in the COPD groups using a magnetic bead panel (Millipore^®).</p><p><strong>Results: </strong>The fold change in NEIL2 mRNA levels were lower in individuals with stable COPD and AECOPD than in controls (0.72 for COPD, p = 0.029; 0.407 for AECOPD, p < 0.001). The difference in NEIL2 mRNA expression between the stable COPD group and AECOPD group was also statistically significant (p < 0.001). The fold change in DNA lesions per 10 kb of DNA was greater in the stable COPD (9.38, p < 0.001) and AECOPD (15.81, p < 0.001) groups than in the control group. The difference in fold change was also greater in the AECOPD group versus stable COPD p < 0.024). Cytokine levels were not significantly different between the COPD groups. NEIL2 levels were correlated with plasma eosinophil levels in the stable COPD group (r = 0.737, p = 0.003).</p><p><strong>Conclusions: </strong>NEIL2 mRNA levels are significantly reduced in individuals with COPD and may exacerbate DNA damage and inflammation. These results suggest a possible mechanism that increases inflammation and oxidative genomic damage in COPD.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"165"},"PeriodicalIF":5.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12039275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}