Lung最新文献

{"title":"Fatty Acids Dysregulation Correlates with Lung Function in Idiopathic Pulmonary Fibrosis.","authors":"Filippo Scialò, Raffaella Pagliaro, Monica Gelzo, Maria Gabriella Matera, Vito D'Agnano, Stefano Sanduzzi Zamparelli, Giuseppe Castaldo, Mario Cazzola, Andrea Bianco, Fabio Perrotta","doi":"10.1007/s00408-025-00852-0","DOIUrl":"10.1007/s00408-025-00852-0","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with a poor survival rate and undefined molecular mechanisms. The identification of reliable biomarkers to help early diagnosis and predict disease progression is crucial for improving patient life. Although many biomarkers have been proposed, there is no consensus on reliable markers for IPF. Alterations in fatty acid (FA) metabolism have drawn increasing attention in the IPF pathogenesis.</p><p><strong>Methods: </strong>This single-center, prospective, cross-sectional study enrolled 35 IPF patients and 24 control participants. Demographic, clinical, and pulmonary function data were collected. FA profiles were compared between the two groups, with statistical analyses including chi-square tests, ANOVA, Spearman's rank correlation, and ROC curve analysis.</p><p><strong>Results: </strong>We found significant differences in serum FA levels between IPF patients and controls. Cis-Palmitoleic acid (26.4 mg/L vs 22.1 mg/L; p = 0.04), oleic acid (457.6 mg/L vs 376.4 mg/L, p = 0.04), and elaidic acid (33.7 mg/dL vs 28.2 mg/L, p = 0.02) were increased in IPF patients, while arachidonic acid (79.7 mg/dL vs 97.9 mg/L, p = 0.01) levels were significantly lower compared to the control group. Spearman's correlation analysis revealed positive correlations between these fatty acids. Notably, arachidonic acid levels showed a positive correlation with FEV1% (r = 0.348; p = 0.043) and FVC% (r = 0.431; p = 0.01), although ROC curve analysis indicated that this did not demonstrate strong diagnostic potential for IPF.</p><p><strong>Conclusion: </strong>In this study, we identified a dysregulation of cis-palmitoleic acid, oleic acid, elaidic acid, and arachidonic acid in IPF patients, indicating alterations in lipid metabolism and inflammatory pathways. Additionally, while arachidonic acid levels correlate with lung function, its diagnostic potential remains uncertain and warrants further evaluation in a larger patient population.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"99"},"PeriodicalIF":3.9,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12521298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286483","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":"Alteration of the Secretome in Airway Epithelial Cells by Air Pollutants: Evidence from an Air-Liquid Interface Model.","authors":"Hankun Lu, Jiahui Xiang, Xiaoyu Zhou, Mingtong Lin, Chuqin Huang, Fang Yi, Zhe Chen, Kefang Lai","doi":"10.1007/s00408-025-00851-1","DOIUrl":"https://doi.org/10.1007/s00408-025-00851-1","url":null,"abstract":"<p><strong>Introduction: </strong>While the structural damage to the airway epithelium from ozone (O₃) or diesel exhaust particles (DEP) is known, the common regulatory mechanisms activated during mixed exposures, which mirror real-world scenarios, remain poorly understood. This study aimed to identify shared molecular pathways initiated by exposure to O₃ and DEP using an in vitro air-liquid interface (ALI) model to understand the initial cellular responses.</p><p><strong>Methods: </strong>Polarized Calu-3 cell monolayers at the ALI were acutely exposed to non-cytotoxic O₃ or DEP. Barrier integrity was assessed via transepithelial electrical resistance (TEER) and FITC-dextran permeability. Gene expression of tight junctions and alarmin cytokines was quantified by qPCR, while the protein level of tight junctions was identified by immunofluorescence. The cellular secretome was comprehensively analyzed using label-free liquid chromatography-tandem mass spectrometry.</p><p><strong>Results: </strong>Both pollutants impaired barrier integrity, evidenced by decreased TEER and increased permeability, and induced a potent inflammatory response via upregulation of alarmin cytokines IL-25, IL-33, and TSLP. Critically, secretome analysis revealed that although O₃ and DEP initiated distinct upstream damage patterns, their responses converged on common downstream pathways, including the activation of Wnt signaling and antigen processing and presentation.</p><p><strong>Conclusion: </strong>Exposure to O₃ and DEP compromises airway epithelial barrier function and triggers a robust alarmin-driven inflammatory response. Our identification of convergent downstream pathways, such as Wnt signaling, provides crucial mechanistic insights into the shared pathophysiology of mixed pollutant exposure. These findings highlight potential therapeutic targets for mitigating the adverse health effects of complex air pollution.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"98"},"PeriodicalIF":3.9,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Healthcare Resource Utilization of Patients with Refractory Chronic Cough Compared to Those with Non-Refractory Chronic Cough.","authors":"Laurent Guilleminault, Clairelyne Dupin, Laurent Portel, Maeva Zysman, Thomas Flament, Pauline Roux, Nadège Costa, Michael Mounié","doi":"10.1007/s00408-025-00853-z","DOIUrl":"https://doi.org/10.1007/s00408-025-00853-z","url":null,"abstract":"<p><strong>Background: </strong>Refractory chronic cough (RCC) significantly impairs patient quality of life and poses a major challenge in clinical management. However, little is known about the healthcare resource utilization (HRU) of patients with RCC.</p><p><strong>Objective: </strong>The goal of our study is to describe the HRU and associated costs of RCC patients and those with non-refractory chronic cough (non-RCC).</p><p><strong>Methods: </strong>Patients with chronic cough were prospectively recruited from 6 centers in France. At 6 months, the patients were classified as having RCC or no RCC. A retrospective analysis was made using the French National Health Insurance Database (SNDS) in order to determine healthcare utilization for the one-year period preceding inclusion at the site and for the one-year period thereafter.</p><p><strong>Results: </strong>Sixty-eight patients were included. Among them, 32 (47%) patients had RCC. There was no difference between groups regarding clinical data apart from cough duration (56.8 ± 59.5 months in the no RCC group vs. 139.3 ± 123.8 months in the RCC group, p = 0.002). Within 1 year prior to inclusion, there was no difference in terms of drug dispensations between the 2 groups. During the 1-year post-inclusion period, a significantly higher proportion of patients with RCC received at least one dispensation of opioids and amitriptyline compared to those with no RCC (8 (25%) vs. 2 (6%) for opioids, p = 0.038 and 14 (44%) vs. 3 (8%) for amitriptyline, p = 0.0015, respectively). Within 1 year after inclusion, more patients with RCC had attended speech pathologist visits in comparison to patients with no RCC (14 (44%) patients vs. 10 (28%) patients, p = 0.21, respectively). Total costs within 12 months prior to inclusion were 3,878€ [2,498 - 5,755€] for patients with no RCC and 5,159€ [3,426 - 7,138€] with RCC, but the difference was not significant. No change occurred in the 1-year period following inclusion.</p><p><strong>Conclusion: </strong>RCC has a high healthcare utilization with substantial costs.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"97"},"PeriodicalIF":3.9,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Down-Regulation of Lactoferrin Expression Induced by Cigarette Smoke can Induce Ferroptosis in COPD.","authors":"Yuxiu Wang, Wenjing Xu, Kaiqi Ren, Jingjing Yang, Lingfeng Min","doi":"10.1007/s00408-025-00849-9","DOIUrl":"https://doi.org/10.1007/s00408-025-00849-9","url":null,"abstract":"<p><strong>Purpose: </strong>Lactoferrin (LTF) plays a crucial role in iron homeostasis, immune response, and inflammation. In the context of chronic obstructive pulmonary disease (COPD), LTF's expression is significantly influenced by environmental factors, particularly cigarette smoke. The pathological mechanism by which cigarette smoke regulates LTF and affects iron metabolism in COPD remains unclear. This study aims to clarify the mechanism therein.</p><p><strong>Methods: </strong>In this study, cigarette smoke extract (CSE) was used to construct mouse and cell models of chronic obstructive pulmonary disease (COPD). Transcriptomic and proteomic tests were performed on the lung tissues of the mouse model of COPD to screen or measure the Hub gene. The interaction network prediction of LTF-related proteins was carried out using the STRING database. The Beas-2B cell model with LTF overexpression and interference was constructed by lentivirus transfection, and then the cell viability, cytotoxicity, lipid reactive oxygen species (ROS), iron ion deposition, and iron-related markers of bronchial epithelial cells after CSE exposure were detected. The morphological changes of mitochondria in bronchial epithelial cells were observed by transmission electron microscopy. The expression levels of ACSL4 and GPX4 proteins in bronchial epithelial cells were detected by Western blotting.</p><p><strong>Results: </strong>The expression of LTF is down-regulated in both lung tissue of the COPD mouse model and bronchial epithelial cells, and it plays a key role in ferroptosis of CSE-induced bronchial epithelial cells. In the LTF-interfered bronchial epithelial cells treated with CSE, ferroptosis-related markers (such as ROS and MDA) were significantly increased, GSH was significantly decreased, mitochondrial volume was reduced, cristae were decreased, the expression of ACSL4 protein was increased, while the expression of GPX4 protein was decreased. Meanwhile, overexpression of LTF can reverse the ferroptosis status of bronchial epithelial cells treated with CSE.</p><p><strong>Conclusion: </strong>Under CSE induction, the decrease in LTF expression level will lead to the accumulation of ferrous ions in bronchial epithelial cells and induce the occurrence of ferroptosis.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"96"},"PeriodicalIF":3.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FUNDC1 Promoted Ferroptosis via JNK Pathway in Cigarette Smoking-Induced Chronic Obstructive Pulmonary Disease.","authors":"Yi Feng, Jiali Weng, Chenfei Li, Qi Liu, Qing Chang, Hai Zhang, Mengnan Li, Kai Wang, Xiaohui Wang, Kian Fan Chung, Ian M Adcock, Feng Li","doi":"10.1007/s00408-025-00850-2","DOIUrl":"https://doi.org/10.1007/s00408-025-00850-2","url":null,"abstract":"<p><strong>Background: </strong>Cigarette smoking (CS), the major risk factor for chronic obstructive pulmonary disease (COPD), induces oxidative stress, mitophagy, and ferroptosis. Because FUN14 domain-containing protein 1 (FUNDC1), a mitophagy receptor, may drive the onset and progression of COPD, we investigated its role in CS-induced ferroptosis in COPD and to explore the underlying cellular signaling mechanisms.</p><p><strong>Methods: </strong>Wild-type (C57BL/6J background) and FUNDC1-knockdown (KD) mice were exposed to CS for 12 weeks. FUNDC1-KD and FUNDC1-overexpressing (OE) alveolar epithelial A549 cells were exposed to CS extracts (CSE) in the presence and absence of the JNK inhibitor, SP6001 (10 mM). Oxidative stress, inflammation, mitochondrial function, and ferroptosis were measured.</p><p><strong>Results: </strong>FUNDC1 expression was increased in lung tissues from COPD patients and CS-exposed mice. CS exposure induced airway inflammation, reduced lung function, and enhanced ferroptosis in mice. FUNDC1-KD prevented CS-induced lung injury in mice. Similarly, CSE exposure up-regulated FUNDC1 expression, promoted ferroptosis, inflammation, oxidative stress, lipid peroxidation, and mitochondrial damage in A549 cells. FUNDC1-KD prevented CSE-induced cellular damage. Transcriptomic data indicated that FUNDC1 mediated ferroptosis through the JNK pathway. These in vitro results were further confirmed by pretreatment with the JNK inhibitor SP6001.</p><p><strong>Conclusion: </strong>FUNDC1 plays an important role in CS-exposed alveolar epithelial cells and in a mouse model of COPD through the JNK-ferroptosis pathway.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"95"},"PeriodicalIF":3.9,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactate and Lactylation in Respiratory Diseases: from Molecular Mechanisms to Targeted Strategies.","authors":"Qi Jia, Quan Yuan, Xiangdong Chen, Zhiqiang Hu","doi":"10.1007/s00408-025-00848-w","DOIUrl":"https://doi.org/10.1007/s00408-025-00848-w","url":null,"abstract":"<p><strong>Introduction: </strong>Lactate has emerged as a multifunctional signaling molecule regulating various physiological and pathological processes. Furthermore, lactylation, a newly identified posttranslational modification triggered by lactate accumulation, plays significant roles in human health and diseases. This study aims to investigate the roles of lactate/lactylation in respiratory diseases.</p><p><strong>Methods: </strong>Comprehensive literature analysis was conducted using PubMed database, utilizing a range of keywords including \"lactate\", \"lactylation\", \"lung\", \"pulmonary\", and \"disease\".</p><p><strong>Results: </strong>Emerging evidence indicates that increased glycolytic flux, resultant lactate accumulation, and elevated lactylation levels play key roles in the pathogenesis of respiratory diseases, including lung cancer, idiopathic pulmonary fibrosis (IPF), acute lung injury/acute respiratory distress syndrome (ALI/ARDS), pulmonary hypertension (PH), and asthma. Under these conditions, the upregulation of glycolytic enzymes and increased lactate transport are observed. Elevated levels of lactate and lactylation profoundly influence multiple biological processes, such as inflammatory responses, immune cell activation, autophagy, ferroptosis, EMT, tumorigenesis, and fibrosis, and lactate/lactylation-targeted therapies have demonstrated therapeutic efficacy against diverse respiratory illnesses.</p><p><strong>Conclusions: </strong>Elevated levels of lactate and lactylation play key roles in the pathogenesis of various respiratory diseases, and lactate/lactylation-targeted therapies appear to be potential therapeutic strategies for these respiratory diseases.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"94"},"PeriodicalIF":3.9,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammatory Consequences of Rhinovirus Infection in Human Epithelial and Neuronal Models.","authors":"Orla M Dunne, Nicola A M Roe, Aurélie Mousnier, S Lorraine Martin, Gerard P Sergeant, Imad About, Ikhlas El-Karim, Fionnuala T Lundy, Lorcan P McGarvey","doi":"10.1007/s00408-025-00846-y","DOIUrl":"10.1007/s00408-025-00846-y","url":null,"abstract":"<p><strong>Introduction: </strong>Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.</p><p><strong>Methods: </strong>PNEs or primary bronchial epithelial cells (PBECs) were infected with the RV-A16 strain. Viral replication was confirmed by viral titration assays, immunofluorescence (IF) for the double-stranded RNA (dsRNA) replication intermediate and western blotting (WB). RNA sequencing was used to determine transcriptomic changes in PNEs, and inflammatory responses were assessed by inflammatory microarray. Calcium mobilisation assays were used to investigate the effect of interleukin-1β (IL-1β) on PNE transient receptor potential (TRP) A1 channel responses.</p><p><strong>Results: </strong>Viral titrations, WB and IF confirm RV-A16 entry and replication in PNEs and PBECs. Gene signatures associated with antiviral immune responses, sensory neuropathies and N-Methyl-D-aspartic acid (NMDA) receptor activity were upregulated in RV infected PNEs. Several cytokines were increased from PNEs and PBECs following RV infection, most notably IL-1β. Treatment of PNEs with IL-1β resulted in heightened TRPA1 channel sensitivity.</p><p><strong>Conclusion: </strong>We report the suitability of an airway neuronal model for the study of the direct effects of RV infection on nerves. RV-induced release of IL-1β from airway epithelium heightens neuronal TRPA1 responses suggesting a mechanism for virus-induced cough hypersensitivity.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"93"},"PeriodicalIF":3.9,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015770","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":"Emerging Therapeutics in COPD: Mapping Innovation to Treatable Traits.","authors":"Mario Cazzola, Vanessa M McDonald, Daiana Stolz, Paola Rogliani, Maria Gabriella Matera","doi":"10.1007/s00408-025-00844-0","DOIUrl":"10.1007/s00408-025-00844-0","url":null,"abstract":"<p><p>Chronic Obstructive Pulmonary Disease (COPD) is a complex, heterogeneous condition characterized by diverse clinical phenotypes and underlying pathobiological mechanisms. Traditional \"one-size-fits-all\" management strategies have limited effectiveness in addressing this heterogeneity. The Treatable Traits (TTs) approach represents a precision medicine paradigm that targets specific, identifiable, and modifiable traits in individual patients, regardless of diagnostic labels. This paper explores the alignment between the TTs framework and emerging pharmacological therapies, with a particular focus on anti-inflammatory agents and bronchodilators currently under investigation. Each drug category is mapped to relevant TTs, such as eosinophilic or neutrophilic inflammation, corticosteroid resistance, chronic bronchitis, and frequent exacerbations. This review highlights the importance of biomarker-driven phenotyping and real-world data in designing TT-based clinical trials. It emphasizes challenges such as trait instability over time, comorbidity clustering, and trial design heterogeneity. Moreover, we advocate for incorporating digital health tools, long-term follow-up, and cost-effectiveness analyses to ensure translational relevance. In conclusion, integrating emerging therapies with the TTs approach holds substantial promise for personalizing COPD management, improving outcomes, and facilitating targeted drug development.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"92"},"PeriodicalIF":3.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959585","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":"Age-Dependent Risk of Bronchial Asthma Exacerbation in Respiratory Syncytial Virus Co-infection.","authors":"Ken Arimura, Keiko Kan-O, Yasuto Sato, Ken Kikuchi, Hitomi Miura, Asako Sato, Mitsuko Kondo, Etsuko Tagaya","doi":"10.1007/s00408-025-00847-x","DOIUrl":"10.1007/s00408-025-00847-x","url":null,"abstract":"<p><strong>Introduction: </strong>Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) are common viral etiologies of respiratory infections. Although co-infection with other respiratory pathogens is frequently observed, its clinical significance remains unclear.</p><p><strong>Methods: </strong>We retrospectively analyzed 57,746 patients who underwent FILMARRAY®, a comprehensive multiplex polymerase chain reaction testing, between November 2020 and March 2023. Clinical features were compared between single infection and co-infection involving RSV or hMPV using χ² or Fisher's exact tests. Multiple logistic regression was performed to identify associations with bronchial asthma (BA) exacerbation, adjusting for age, sex, testing period, and RSV co-infection.</p><p><strong>Results: </strong>Among RSV-positive patients, co-infection was associated with higher prevalence of BA history, wheeze, BA exacerbation, combined BA history and exacerbation, systemic steroid use, and age under 6 years compared to that with single infection. RSV co-infection with coronavirus, parainfluenza virus, adenovirus, and rhinovirus/enterovirus was particularly associated with BA exacerbation. Age under 6 years and RSV co-infection were identified as independent risk factors for BA exacerbation using multiple logistic regression. In contrast, no associations were observed in the hMPV co-infection.</p><p><strong>Conclusion: </strong>RSV co-infection with other respiratory viruses increases the risk of BA exacerbation, especially in age under 6 years patients. Given the proven efficacy of RSV vaccine for adults and monoclonal antibody for high-risk children in preventing RSV-related lower respiratory tract disease, RSV-targeted prevention strategies for younger children appear effective in reducing respiratory disease burden.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"91"},"PeriodicalIF":3.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959606","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":"Changes in Lung Function and Patient-Reported Outcomes in Patients with Idiopathic Pulmonary Fibrosis.","authors":"Jamie L Todd, Megan L Neely, Anne S Hellkamp, Daniel A Culver, Justin M Oldham, Peide Li, Divya C Patel, Scott M Palmer","doi":"10.1007/s00408-025-00845-z","DOIUrl":"https://doi.org/10.1007/s00408-025-00845-z","url":null,"abstract":"<p><p>We evaluated relationships between changes in lung function and changes in patient-reported outcomes (PROs) in 736 patients with idiopathic pulmonary fibrosis (IPF) enrolled in the IPF-PRO Registry. Weak correlations were observed between changes in percent predicted values for forced vital capacity or diffusing capacity of the lungs (DLco) and changes in St George's Respiratory Questionnaire (SGRQ) total and activity scores and the 12-item Short Form Survey (SF-12) physical component summary score over 12-month periods. Patients who had a deterioration in SGRQ activity score or SF-12 PCS score of ≥ 5 units had numerically larger declines in lung function than other patients, but the differences were small. The weak relationships observed between changes in lung function and changes in PROs underscore the importance of evaluating both changes in lung function and changes in HRQL in clinical practice and clinical trials.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"90"},"PeriodicalIF":3.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959637","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}