Respiratory Research最新文献

{"title":"Body composition, maximal fitness, and submaximal exercise function in people with interstitial lung disease.","authors":"Owen W Tomlinson, Anna Duckworth, Laura Markham, Rebecca L Wollerton, Michael Gibbons, Chris J Scotton, Craig A Williams","doi":"10.1186/s12931-025-03195-9","DOIUrl":"10.1186/s12931-025-03195-9","url":null,"abstract":"<p><strong>Background: </strong>Cardiopulmonary exercise testing (CPET) is feasible, valid, reliable, and clinically useful in interstitial lung disease (ILD). However, maximal CPET values are often presented relative to body mass, whereas fat-free mass (FFM) may better reflect metabolically active muscle during exercise. Moreover, despite the value of maximal parameters, people with ILD do not always exercise maximally and therefore clinically relevant submaximal parameters must be identified. Therefore, this study assessed peak oxygen uptake (VO_2peak) relative to FFM, identifying the validity of common scaling techniques; as well as characterising the oxygen uptake efficiency slope (OUES) and plateau (OUEP) as possible submaximal parameters.</p><p><strong>Methods: </strong>Participants with ILD underwent assessment of body composition and CPET via cycle ergometry during a single study visit. To determined effectiveness of scaling for body size, both body mass and FFM were scaled using ratio-standard (X/Y) and allometric (X/Y^b) techniques. Pearsons's correlations determined agreement between OUES, OUEP, and parameters of lung function. Cohens kappa (κ) assessed agreement between OUES, OUEP and VO_2peak.</p><p><strong>Results: </strong>A total of 24 participants (7 female; 69.8 ± 7.5 years; 17 with idiopathic pulmonary fibrosis) with ILD completed the study. Maximal exercise parameters did not require allometric scaling, and when scaled to FFM, it was shown that women have a significantly higher VO_2peak than men (p = 0.044). Results also indicated that OUEP was significantly and positively correlated with DL_CO (r = 0.719, p < 0.001), and held moderate agreement with VO_2peak (κ = 0.50, p < 0.01).</p><p><strong>Conclusion: </strong>This study identified that ratio-standard scaling is sufficient in removing residual effects of body size from VO_2peak, and that VO_2peak is higher in women when FFM is considered. Encouragingly, this study also identified OUEP as a possible alternative submaximal marker in people with ILD, and thus warrants further examination.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"123"},"PeriodicalIF":5.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11966908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774657","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":"Burden of non-COVID-19 lower respiratory infections in China (1990-2021): a global burden of disease study analysis.","authors":"Manyu Li, Zeyu Song, Wenjun Wan, Haiwei Zhou","doi":"10.1186/s12931-025-03197-7","DOIUrl":"10.1186/s12931-025-03197-7","url":null,"abstract":"<p><strong>Background: </strong>The assessment of lower respiratory infection (LRI) mortality, incidence, and responsible pathogens in China provides a scientific basis for the prevention and management of LRI, especially for evaluating the impact of coronavirus disease 2019 (COVID-19). We provide a national estimate of the non-COVID-19 LRI burden and trends on people from 1990 to 2021 based on Global Burden of Disease (GBD) study 2021.</p><p><strong>Methods: </strong>We estimated China's mortality, incidence, disability-adjusted life years (DALYs), risk factors and aetiology attribution for LRI without including COVID-19 by using the estimated data of GBD study 2021. Mortality, incidence, DALYs, risk factors and aetiology were stratified by sex and age. Trends were evaluated using estimated annual percentage change.</p><p><strong>Results: </strong>In 2021, it is estimated that there were 206930.22 deaths (95% uncertainty interval [UI]: 171260.88-251990.47), with all-age mortality rate of 14.54 deaths (95% UI: 12.04-17.71) per 100,000 population. Compared to 2019, the all-age mortality rate had a 3.60% increase. Analyzing risk factors from 1990 to 2021, we found that the percentage of DALYs attributed to tobacco increased from 7.44% (95% UI: 1.26-15.72%) to 22.14% (95% UI: 3.28-38.41%), and that attributable to ambient particulate matter pollution increased from 19.84% (95% UI: 8.79-30.20%) to 32.72% (95% UI: 22.78-41.77%). The leading cause of mortality from LRIs remains Streptococcus pneumoniae from 1990 to 2021. However, the proportions of viral infections decreased. Compared to 2019, the proportion of deaths in 2021 caused by Influenza decreased from 13.03 to 2.70%, and the proportion of deaths due to RSV decreased from 2.21 to 0.41%.</p><p><strong>Conclusions: </strong>In China, substantial progress has been made in reducing LRI mortality, yet LRIs have remained a threat in China from 1990 to 2021. During the COVID-19 pandemic, the mortality attributable to Influenza and RSV declined. Effective vaccines and treatments targeted at the main pathogens of LRI are important.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"125"},"PeriodicalIF":5.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11966843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774677","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":"The effect of a post-bronchodilator FEV₁/FVC < 0.7 on COPD diagnosis and treatment: a regression discontinuity design.","authors":"Alexander T Moffett, Scott D Halpern, Gary E Weissman","doi":"10.1186/s12931-025-03198-6","DOIUrl":"10.1186/s12931-025-03198-6","url":null,"abstract":"<p><strong>Background: </strong>Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend the diagnosis of chronic obstructive pulmonary disease (COPD) only in patients with a post-bronchodilator forced expiratory volume in 1 s to forced vital capacity ratio (FEV₁/FVC) less than 0.7. However the impact of this recommendation on clinical practice is unknown.</p><p><strong>Objective: </strong>To estimate the effect of a documented post-bronchodilator FEV₁/FVC < 0.7 on the diagnosis and treatment of COPD.</p><p><strong>Design: </strong>We used a regression discontinuity design to measure the effect of a post-bronchodilator FEV₁/FVC < 0.7 on COPD diagnosis and treatment.</p><p><strong>Participants: </strong>Patients included in a national electronic health record database who were 18 years of age and older and had a clinical encounter between 2007 and 2022 in which a post-bronchodilator FEV₁/FVC value was documented.</p><p><strong>Main measures: </strong>An encounter was associated with a COPD diagnosis if an international classification of disease code for COPD was assigned, and was associated with COPD treatment if a prescription for a medication commonly used to treat COPD was filled within 90 days.</p><p><strong>Results: </strong>Among 27,817 clinical encounters, involving 18,991 patients, a post-bronchodilator FEV₁/FVC < 0.7 was present in 14,876 (53.4%). The presence of a documented post-bronchodilator FEV₁/FVC < 0.7 increased the probability of a COPD diagnosis by 6.0% (95% confidence interval [CI] 1.1-10.9%) from 38.0% just above the 0.7 cutoff to 44.0% just below this cutoff. The presence of a documented post-bronchodilator FEV₁/FVC < 0.7 had no effect on the probability of COPD treatment (-2.1%, 95% CI -7.2 to 3.0%).</p><p><strong>Conclusions: </strong>The presence of a documented post-bronchodilator FEV₁/FVC < 0.7 had only a small effect on the diagnosis of COPD and no effect on corresponding treatment decisions.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"122"},"PeriodicalIF":5.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765660","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":"Describing the burden of moderate exacerbations in patients with asthma from the Extended Salford Lung Study (Ext-SLS): a retrospective cohort study.","authors":"Emma Goodall, Kieran J Rothnie, Beade Numbere, Shiyuan Zhang, Chris Compton, Robert Wood, Theo Tritton, Rosie Wild, Mark Small, Jørgen Vestbo, Ashley Woodcock","doi":"10.1186/s12931-025-03199-5","DOIUrl":"10.1186/s12931-025-03199-5","url":null,"abstract":"<p><strong>Background: </strong>There is a need for real-world data describing the frequency and impact of moderate asthma exacerbations in patients receiving inhaled corticosteroids/long-acting β₂-agonists (ICS/LABA). The Salford Lung Study (SLS) and associated extension study (Ext-SLS) evaluated ICS/LABA versus existing maintenance therapy in adults with asthma. This analysis assessed the impact of moderate exacerbations in patients from the Ext-SLS.</p><p><strong>Methods: </strong>This retrospective cohort study analysed linked primary and secondary care and patient questionnaire data from patients enrolled in the Ext-SLS (indexed April 2018-May 2019). Primary outcome was number of self-reported moderate asthma exacerbations 12 months pre-index, overall, by maintenance treatment class and asthma control status at index, using the Asthma Control Test (ACT; poor [< 16], somewhat controlled [16-18], and controlled [> 19]) and 6-item Asthma Control Questionnaire (ACQ-6; uncontrolled [≥ 1.50], partially controlled [> 0.75-<1.50], and controlled [≤ 0.75]). Secondary outcomes included index ACT and ACQ-6 score, healthcare resource utilisation (HCRU) and direct costs 12 months pre- and post-index, stratified by self-reported moderate exacerbation frequency pre-index.</p><p><strong>Results: </strong>Of 485 patients with ≥ 12 months' pre-index data, 86.6% (n = 420) self-reported moderate exacerbations, with similar frequency irrespective of maintenance treatment class (66.7-100.0%; ICS/LABA: 85.4%). Numerically greater proportions of patients self-reported a moderate exacerbation in the 12 months pre-index in ACT poor-control (n = 110/115 [95.7%]) and ACQ-6-uncontrolled (n = 200/210 [95.3%]) versus ACT- and ACQ-6-controlled (n = 205/260 [78.8%], n = 105/145 [72.4%]) groups. Symptom control worsened with increasing exacerbation frequency: mean (SD) ACT scores were 21.8 (3.3) and 15.7 (4.4) for patients with 0 or ≥ 7 events, respectively; mean (SD) ACQ-6 scores followed the same trend. Direct costs and HCRU increased with pre-index exacerbation frequency; mean (SD) all-cause and asthma-related total costs were £1509 (£2384) and £717 (£1459) for patients with no moderate exacerbations 12 months pre-index and £2002 (£2058) and £1086 (£1538) for patients with ≥ 7 exacerbations; similar trends occurred over 12 months post-index.</p><p><strong>Conclusions: </strong>Patients with asthma experience frequent moderate exacerbations, which are associated with poor asthma control, increased HCRU and costs, emphasising the poor quality of life patients experience. Tackling poor adherence, risk behaviour, and comorbidities as well as holistic management and medication review are needed.</p><p><strong>Clinical trial details: </strong>Registered on clinicaltrials.gov: NCT03152669, 12 May 2017.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"121"},"PeriodicalIF":5.8,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744300","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":"Hidden in plain sight: the impact of human rhinovirus infection in adults.","authors":"Tommaso Morelli, Anna Freeman, Karl J Staples, Tom M A Wilkinson","doi":"10.1186/s12931-025-03178-w","DOIUrl":"10.1186/s12931-025-03178-w","url":null,"abstract":"<p><strong>Background: </strong>Human rhinovirus (HRV), a non-enveloped RNA virus, was first identified more than 70 years ago. It is highly infectious and easily transmitted through aerosols and direct contact. The advent of multiplex PCR has enhanced the detection of a diverse range of respiratory viruses, and HRV consistently ranks among the most prevalent respiratory pathogens globally. Circulation occurs throughout the year, with peak incidence in autumn and spring in temperate climates. Remarkably, during the SARS-CoV-2 pandemic, HRV transmission persisted, demonstrating its resistance to stringent public health measures aimed at curbing viral transmission.</p><p><strong>Main body: </strong>HRV is characterised by its extensive genetic diversity, comprising three species and more than 170 genotypes. This diversity and substantial number of concurrently circulating strains allows HRVs to frequently escape the adaptive immune system and poses formidable challenges for the development of effective vaccines and antiviral therapies. There is currently a lack of specific treatments. Historically, HRV has been associated with self-limiting upper respiratory infection. However, there is now extensive evidence highlighting its significant role in severe lower respiratory disease in adults, including exacerbations of chronic airway diseases, such as asthma and chronic obstructive pulmonary disease (COPD), as well as pneumonia. These severe manifestations can occur even in immunocompetent individuals, broadening the clinical impact of this ubiquitous virus. Consequently, the burden of rhinovirus infections extends across various healthcare settings, from primary care to general hospital wards and intensive care units. The impact of HRV in adults, in terms of morbidity and healthcare utilisation, rivals that of the other major respiratory viruses, including influenza and respiratory syncytial virus. Recognition of this substantial burden underscores the critical need for novel treatment strategies and effective management protocols to mitigate the impact of HRV infections on public health.</p><p><strong>Conclusion: </strong>This review examines the epidemiology, clinical manifestations, and risk factors associated with severe HRV infection in adults. By drawing on contemporary literature, we aim to provide a comprehensive overview of the virus's significant health implications. Understanding the scope of this impact is essential for developing new, targeted interventions and improving patient outcomes in the face of this persistent and adaptable pathogen.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"120"},"PeriodicalIF":5.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744305","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":"Harmine alleviates LPS-induced acute lung injury by inhibiting CSF3-mediated MAPK/NF-κB signaling pathway.","authors":"Yihui Zhai, Kejie Chen, Zichuang Xu, Xiaojian Chen, Jiaying Tong, Yeying He, Chaoyue Chen, Meiqing Ding, Guang Liang, Xiaohui Zheng","doi":"10.1186/s12931-025-03196-8","DOIUrl":"10.1186/s12931-025-03196-8","url":null,"abstract":"<p><strong>Background: </strong>Acute lung injury (ALI) is a life-threatening inflammatory lung disease that lacks safe and effective treatment strategies. Harmine, an alkaloid derived from Peganum harmala L plants, exhibits anti-inflammatory activity. However, the protective effect of harmine against ALI and its underlying mechanism remain unknown. This study aimed to elucidate the therapeutic effects and molecular mechanisms of harmine against ALI.</p><p><strong>Methods: </strong>The therapeutic effects of harmine were assessed in LPS-induced ALI mice. Serum, bronchoalveolar lavage fluid (BALF), lung tissues were routinely analyzed to evaluated disease severity. The anti-inflammatory mechanism was elucidated in LPS-simulated RAW264.7 cells using a series assays, including RNA-seq, gene silencing, immunofluorescence, western blotting, co-immunoprecipitation and bioinformatic analysis. The biological safety of harmine was determined both in vitro and in vivo through cytotoxicity test, long-term cell proliferation test, acute toxicity test in mice, and assessments of liver and kidney function and structural changes.</p><p><strong>Results: </strong>The results showed that harmine inhibited the expression and secretion of LPS-induced inflammatory factors (IL-6, IL-1β and TNF-α) and reduced inflammatory cell infiltration in the lungs, resulting in alleviated LPS-induced histopathological changes and injury in mice. Mechanically, the findings revealed that harmine does not disrupt the TLR4-MD2 interaction but instead attenuates inflammation by suppressing CSF3 transcription and expression, leading to the inhibition of the MAPK/NF-κB signaling pathway activation induced by LPS stimulation. Additionally, both in vitro and in vivo studies demonstrated that harmine administration does not exhibit obvious cytotoxicity or long-term cell proliferation inhibition, nor does it cause functional or organic lesions the liver and kidney in mice, or other acute toxic effects.</p><p><strong>Conclusions: </strong>These findings elucidated that the anti-inflammatory activity of harmine was achieved through the CSF3-mediated inactivation of the MAPK/NF-κB signaling pathway, suggesting that harmine could serve as a promising therapeutic drug for ALI and other inflammatory diseases.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"119"},"PeriodicalIF":5.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744304","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":"Effects of urban airborne particulate matter exposure on the human upper respiratory tract microbiome: a systematic review.","authors":"Sonia Arca-Lafuente, Beatriz Nuñez-Corcuera, Rebeca Ramis, Spyros Karakitsios, Denis Sarigiannis, Saúl García Dos Santos, Amanda Fernández-Rodríguez, Verónica Briz","doi":"10.1186/s12931-025-03179-9","DOIUrl":"10.1186/s12931-025-03179-9","url":null,"abstract":"<p><p>Exposure to air pollutants has a direct impact on human health, resulting in increased mortality rates. Airborne particulate matter (PM) has major adverse effects on health and can be classified as high-risk respiratory particles (fine/PM_2.5, aerodynamic diameter < 2.5 µm) or thoracic particles (coarse/PM₁₀, aerodynamic diameter < 10 µm). In addition, airborne PM can carry microbial communities that alter the commensal microbiota and lead to dysbiosis. Our aim was to synthesize the current research evidence describing the association between air pollution exposure and the microbiome composition of the upper respiratory tract (URT) of the adult population. In this work, a systematic search of the PubMed, EMBASE and Scopus databases was conducted. A total of 9 studies published from 2018 to 2023 were included. 66.5% of the participants were exposed to PM_2.5 concentrations higher than 40 µg/m³, and data showed that PM_2.5 atmospheric levels were positively correlated with PM₁₀ (r_s = 0.95, p < 0.001). All the reviewed studies performed 16S rRNA sequencing of the V3-V4 region from URT samples, using different methods. Overall, evidence of URT microbiome alterations after high PM exposure was observed, with seasonal and geographical influence. Discordant findings were found about bacterial diversity, with a predominant decrease after exposure to high PM levels. Regarding microbiome composition, the relative abundance of the Actinobacteria phylum declined following exposure to high levels of PM, but that of Bacteroidetes and Fusobacteria increased. The studies showed a low-middle risk of bias due to heterogeneity regarding sample processing, sequencing methods, and confounder control. To confirm the observed evidence of an association between PM levels and alterations in the URT microbiome, we strongly recommend that future research work be conducted in accordance with standard guidelines for reporting microbiome studies. In summary, the entry of fine and coarse particles into the URT is associated with microbial dysbiosis, increasing the risk of developing respiratory diseases and allergies.Prospero registration: This systematic review was registered on PROSPERO (#CRD42023416230).</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"118"},"PeriodicalIF":5.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744303","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":"Correction to: Epidemiology, ventilation management and outcomes of COVID-19 ARDS patients versus patients with ARDS due to pneumonia in the Pre-COVID era.","authors":"Fleur-Stefanie L I M van der Ven, Siebe G Blok, Luciano C Azevedo, Giacomo Bellani, Michela Botta, Elisa Estenssoro, Eddy Fan, Juliana Carvalho Ferreira, John G Laffey, Ignacio Martin-Loeches, Ana Motos, Tai Pham, Oscar Peñuelas, Antonio Pesenti, Luigi Pisani, Ary Serpa Neto, Marcus J Schultz, Antoni Torres, Anissa M Tsonas, Frederique Paulus, David M P van Meenen","doi":"10.1186/s12931-025-03176-y","DOIUrl":"https://doi.org/10.1186/s12931-025-03176-y","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"117"},"PeriodicalIF":5.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744352","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":"Risk of acute exacerbation of chronic obstructive pulmonary disease after COVID-19 recovery: a nationwide population-based cohort study.","authors":"Sang Hyuk Kim, Hyun Lee, Min Ji Kim, Youlim Kim, Kyung Hoon Min, Kwang Ha Yoo, Jong Seung Kim, Ji-Yong Moon","doi":"10.1186/s12931-025-03123-x","DOIUrl":"10.1186/s12931-025-03123-x","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is associated with severe Coronavirus disease 2019 (COVID-19) outcomes. However, it is uncertain whether the risk of acute exacerbation of COPD (AECOPD) increases after recovering from COVID-19.</p><p><strong>Methods: </strong>This study included 2,118 individuals with COPD from the Korea National Health Insurance Service database who were also diagnosed with COVID-19. Matched controls were chosen using 1:1 propensity score (PS) matching. We compared the risk of AECOPD after COVID-19 recovery between the COVID-19 cohort and matched controls between October 8, 2020, and December 31, 2021, using PS-matched Cox proportional hazard regression models.</p><p><strong>Results: </strong>During a median follow-up of 62 days (interquartile range, 29-179 days), including a median of 14 days of recovery time after COVID-19, 68 people (5.6%) in the COVID-19 cohort and 50 (3.9%) in the matched control group experienced AECOPD. Compared to the matched controls, the COVID-19 cohort had a significantly higher risk of overall AECOPD (hazard ratio [HR] = 1.45, 95% confidence interval [CI] = 1.09-1.92). This increased risk was particularly evident for severe AECOPD among individuals who had severe COVID-19 within the first 30days post-recovery (aHR = 8.14, 95% CI = 3.32-19.97). When classified by COVID-19 severity, while severe COVID-19 significantly increased this risk (aHR = 2.97, 95% CI = 2.15-4.11), non-severe COVID did not significantly influence the risk of AECOPD, regardless of time duration or exacerbation severity.</p><p><strong>Conclusion: </strong>Individuals with COPD who had severe COVID-19 have increased risk of AECOPD after COVID-19 recovery, especially within the first 30 days after COVID-19 recovery.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"116"},"PeriodicalIF":5.8,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143732633","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":"Molecular mechanisms and therapeutic targets of acute exacerbations of chronic obstructive pulmonary disease with Pseudomonas aeruginosa infection.","authors":"Zhiwei Lin, Shuang Liu, Ke Zhang, Tianyu Feng, Yewei Luo, Yu Liu, Baoqing Sun, Luqian Zhou","doi":"10.1186/s12931-025-03185-x","DOIUrl":"10.1186/s12931-025-03185-x","url":null,"abstract":"<p><strong>Background: </strong>Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of global mortality, with acute exacerbations of COPD (AECOPD) significantly increasing the disease's morbidity and mortality. Among the pathogens implicated in AECOPD, Pseudomonas aeruginosa (P. aeruginosa) is increasingly recognized as a major co-infecting bacterium. Despite its clinical importance, the molecular mechanisms and therapeutic targets underlying AECOPD with P. aeruginosa infection remain inadequately understood.</p><p><strong>Methods: </strong>We employed a multi-omics approach, integrating proteomic analyses of bronchoalveolar lavage fluid (BALF) and plasma with transcriptomic analysis of peripheral blood. A discovery cohort of 40 AECOPD with P. aeruginosa infection patients and 20 healthy controls was analyzed, followed by validation in an independent cohort of 20 patients and 10 controls. Differentially expressed proteins (DEPs) and genes (DEGs) were identified and subjected to protein-protein interaction (PPI) network analysis, weighted gene co-expression network analysis (WGCNA), and immune infiltration analysis. Molecular docking simulations were conducted to explore potential therapeutic agents.</p><p><strong>Results: </strong>Our integrative analysis identified key biomarkers, which played critical roles in oxidative stress and neutrophil extracellular trap (NET) formation, both of which were pivotal in the pathogenesis of AECOPD with P. aeruginosa infection. The combined analysis of BALF, plasma, and peripheral blood underscored the interplay between local lung changes and systemic immune responses. Functional enrichment analyses highlighted significant pathways related to bacterial defense, inflammation, and immune activation. Validation in an independent cohort confirmed the diagnostic value of three key proteins (AZU1, MPO, and RETN), with high area under the curve (AUC) values in ROC analyses. Molecular docking indicated strong binding affinities of these proteins with Pioglitazone and Rosiglitazone, suggesting potential therapeutic utility.</p><p><strong>Conclusions: </strong>This study provides a comprehensive understanding of the molecular mechanisms underlying AECOPD with P. aeruginosa infection, highlighting the pivotal roles of oxidative stress and NET formation in disease progression. The identified biomarkers offer promising diagnostic and therapeutic targets. Our findings pave the way for novel strategies to improve outcomes for AECOPD patients with P. aeruginosa infection. While the study design limits our ability to establish causality, these results provide important insights that warrant further investigation, particularly through longitudinal studies, to confirm the specific contributions of P. aeruginosa in exacerbations.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"115"},"PeriodicalIF":5.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721973","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}