RESPIRATORY RESEARCH呼吸研究
RESPIRATORY RESEARCH(英文缩写 RESP RES),ISSN 1465-9921,eISSN 1465-993X,中文译名:呼吸研究 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
RESPIRATORY RESEARCH 最新收录文献
-
2. Roles of alarmins in human small airways are independent of immune cells.
PMID:日期:2026-09-28该文献暂无摘要。
-
3. The Tie-2 agonist PMC-403 inhibits endothelial damage induced by e-cigarette vapor or LPS.
PMID:日期:2026-09-26The use of e-cigarettes is currently increasing despite potential harmful effects of e-cigarettes. Acute e-cigarette exposure may cause endothelial damage thereby contributing to acute lung injury or vascular dysfunction after chronic use. These effects may be enhanced by concomitant inflammatory stimuli. We investigated the acute effect of e-cigarette vapor (ECV) with or without concomitant lipopolysaccharide (LPS) stimulation on endothelial cell function in vitro and on vascular permeability in isolated lungs. Further potentially protective effects of the Tie2 agonist PMC-403 were studied. Human umbilical cord endothelial cells (HUVECs) were cultured with different types of ECV extracts (ECVE) and/or LPS, and endothelial activation was determined in vitro by measuring secreted protein and mRNA levels of angiopoietin-2 (Angpt-2) and soluble Tie2 (sTie2). Barrier dysfunction was analyzed by continuous transendothelial electrical resistance (TER) measurements using electric cell-substrate impendence sensing (ECIS). An ex vivo isolated mouse lung model was used to analyze endothelial permeability and edema formation upon intratracheal ECV exposure. The Tie2 agonist PMC-403 was applied in vitro and ex vivo and its effect on endothelial permeability was determined. Angpt-2 secretion and transcription were significantly increased in HUVECs after 24h stimulation with nicotine-containing ECVE (ECVE), but not nicotine-free ECVE. Preincubation with ECVE significantly enhanced the LPS-induced increase of Angpt-2 secretion. On a functional level, ECVE exposure resulted in greater susceptibility to an LPS-induced increase in endothelial barrier permeability. In isolated, ventilated and perfused mouse lungs intratracheal nicotine-containing ECV application (ECV) or LPS application via the perfusate increased endothelial permeability and lung edema, however, combination of ECV and LPS did not have additive effects. A novel synthetic Tie2 agonist PMC-403 decreased both the LPS-induced loss of endothelial barrier function in vitro and the ECV- or LPS-induced endothelial barrier dysfunction ex vivo. ECV exposure increased endothelial permeability and lung edema formation in an angiopoietin/Tie2 dependent manner ex vivo, and susceptibility to LPS stimulation in vitro. We identified the Tie2 activating anti-permeability agent PMC-403 as a potential therapeutic agent of acute lung injury in this context.
-
5. Early-life serum protein profiles associated with bronchopulmonary dysplasia in extremely preterm infants.
PMID:日期:2026-09-18Bronchopulmonary dysplasia (BPD) affects the most immature preterm infants and can result in long term pulmonary morbidity. Yet, how prenatal and neonatal exposures perturb early proteome maturation and contribute to BPD pathogenesis remains unclear. In a cohort of 176 extremely preterm infants (born < 28 weeks gestational age) previously enrolled in a multicenter randomized trial, 825 longitudinal serum samples were collected the first five postnatal weeks. 98 of 176 infants were defined as having BPD based on need for any respiratory support at 36 weeks postnatal age. Proteomic analysis was conducted using proximity extension assay from Olink. Mixed models, adjusted for gestational age, study center, and randomization group, also including an interaction term between BPD and time, were used to analyse differences in longitudinal protein trajectories by BPD status. False discovery rate correction was applied. Out of 538 analysed proteins, 108 exhibited distinct longitudinal trajectories in infants with BPD. Among the top significant proteins, several have previously been associated with BPD (e.g. lower Secretoglobin family 3A member 1 [SCGB3A1] and higher intercellular adhesion molecule 1 [ICAM-1]), while others represent novel findings (e.g. lower Leukocyte differentiation antigen CD84). Network and functional enrichment analysis revealed involvement in multiple biological processes, with many of the top significant proteins related to immune function. Some proteins showed associations specific to more mature infants (e.g. Stem cell factor). Differences in early serum protein trajectories are evident in infants who develop BPD. Our findings suggest associations consistent with proposed pathophysiological mechanisms. Clinical factors likely interact with immune-related proteins in the development of BPD. Mitigating inflammation by stabilising potential protective factors could be important for BPD prevention. ClinicalTrial.gov identifier NCT03201588.
-
6. Aryl hydrocarbon receptor (AhR) regulates organic dust and organic dust-associated bacterial extracellular vesicles-induced airway inflammation via ROS-dependent NFκB and STAT3 activation.
PMID:日期:2026-09-10Exposure to agricultural organic dust increases the risk of respiratory diseases. Aryl hydrocarbon receptor (AhR), a transcription factor activated by environmental chemicals and endogenous metabolites, regulates immune and inflammatory responses, but its role in organic dust-induced lung inflammation is not known. Our study elucidated mechanisms by which AhR modulates bronchial epithelial cell inflammatory responses induced by poultry farm organic dust extract (DE) and organic dust-associated (OD) bacterial extracellular vesicles (EVs). The role of AhR in the DE- and OD-bacterial EVs-mediated inflammatory responses in Beas2B bronchial epithelial cells was investigated using siRNA knockdown. AhR expression and nuclear translocation, reactive oxygen species (ROS), and inflammatory mediator (pro-IL-1β, ICAM-1, IL-6, IL-8) levels were evaluated by western immunoblotting, immunostaining, DCFDA labeling, real-time qRT-PCR, and ELISA. The induction of lung inflammatory cytokines by OD-bacterial EVs was assessed by ELISA in AhR knockout mice. DE and OD-bacterial EVs increased AhR protein expression and nuclear translocation in a time-dependent manner in Beas2B cells. AhR knockdown reduced ROS and NFκB activation but modulated STAT3 differentially, suppressing DE-induced activation while enhancing OD-bacterial EV-induced activation. Nevertheless, AhR knockdown attenuated the induction of inflammatory mediators by DE and OD-bacterial EVs. Inhibition of NOX, XO, NFκB, and STAT3 attenuated AhR increase by DE- and OD-bacterial EVs. Studies in AhR knockout mice demonstrated that AhR regulates lung inflammatory cytokines in a sex-specific manner. AhR is a critical modulator of organic dust-induced lung inflammation, potentially driven by a positive feedback loop involving ROS and NFκB/STAT3. Targeting the AhR pathway offers a therapeutic strategy for respiratory diseases afflicting agricultural workers.
-
7. Respiratory symptoms up to 18 months after COVID-19 - a longitudinal observational study.
PMID:日期:2026-09-09This study aimed to identify, analyse and compare adults with and without respiratory symptoms over time after COVID-19 and identify predictors of persistent respiratory symptoms, in hospitalised and non-hospitalised patients. Participants were recruited at the Post COVID-19 clinic at Karolinska University hospital, Sweden, between May 2020 until December 2022, with longitudinal data collected until February 2025. Data from medical records and two clinical follow-up visits were analysed. Participants were categorised based on presence or absence of self-reported respiratory symptoms. Clinical outcomes included physical function, patient-reported outcomes, lung function and other clinically relevant parameters. A total of 963 out of 1976 participants were included, of whom 760 (79%) were identified with respiratory symptoms and 203 (21%) were not at first follow-up visit. The respiratory symptom group showed poorer physical function and worse patient-reported outcomes at the first follow-up (adjusted p < 0.05). Lung function was generally preserved, although diffusing lung capacity for carbon monoxide (DLCO) was lower in the respiratory symptom group (79% vs 84%, adjusted p < 0.05). Both groups improved over time, and the magnitude of change did not differ significantly between groups. However, participants in the respiratory symptom group remained more impaired across several outcomes at follow-up. Presence of respiratory symptoms at the first follow-up visit was the strongest independent predictor of belonging to the respiratory symptom group at second follow-up visit (OR 5.31, 95% CI 2.74-10.89). Respiratory symptoms after acute COVID-19 were highly prevalent and were associated with poorer clinical outcomes, despite similar recovery over time. Further research is needed to better clarify underlying mechanisms and to guide targeted rehabilitation strategies.
-
8. Prophylactic cranial irradiation versus active MRI surveillance for limited-stage small-cell lung cancer achieving response after chemoradiotherapy: a protocol for a randomized, controlled, multicenter, phase III trial.
8. 预防性颅脑照射对比主动MRI监测用于放化疗后达到缓解的局限期小细胞肺癌：一项随机、对照、多中心、III期试验方案PMID:日期:2026-09-08Prophylactic cranial irradiation (PCI) is the standard preventive strategy for limited-stage small-cell lung cancer (LS-SCLC). However, the evidence supporting this strategy is largely based on the pre-MRI era. With the advancement of modern MRI and treatment techniques, the survival benefit of PCI remains unclear, particularly given the potential for neurocognitive toxicity to impair quality of life. This study aims to re-evaluate the value of PCI in contemporary LS-SCLC patients and investigate whether active MRI surveillance is non-inferior to PCI regarding overall survival (OS). This is a prospective, randomized, multicenter, phase III trial, enrolling patients with LS-SCLC who achieve complete response (CR) or partial response (PR) after platinum-based chemoradiotherapy. Participants will be randomly assigned (1:1) to receive either PCI or active MRI surveillance. The primary endpoint is OS. Secondary endpoints include 1- and 3-year OS rates, progression-free survival (PFS), brain metastasis rate, and neurocognitive function. Exploratory analyses will integrate clinical characteristics with the longitudinal kinetics of tumor biomarkers in collected peripheral blood to identify patient subgroups who are more likely to benefit from PCI. This study will re-evaluate the role of PCI in the MRI era for LS-SCLC. If active MRI surveillance proves non-inferior, it may provide evidence supporting a less intensive management approach that could potentially reduce treatment-related neurotoxicity and preserve quality of life. Furthermore, our trial aims to identify patient subgroups that derive a clinical benefit from PCI, and leverage serial biomarker dynamics to guide personalized clinical management for LS-SCLC patients. This trial is registered at ClinicalTrials.gov (NCT04829708).
-
9. Current smoking and COPD are associated with differentiation-dependent secretory and inflammatory programs in airway basal cells.
PMID:日期:2026-08-29Persistent airway epithelial abnormalities contribute to chronic obstructive pulmonary disease (COPD), but it remains unclear whether smoking- and COPD-associated epithelial remodeling is retained in airway basal cells and transmitted during differentiation. We determined whether current smoking and COPD are associated with methylation-linked regulatory programs in airway basal cells that shape epithelial differentiation in patient-derived bronchial organoids. We integrated DNA methylation profiling and bulk transcriptomics in patient-derived airway basal cells and matched three-dimensional bronchial organoids. Methylation-defined gene sets were mapped to organoid epithelial cell states using single-cell RNA-seq and contextualized with publicly available airway epithelial datasets. In this exploratory cohort, current smoking was associated with a predominant shift toward promoter hypomethylation in airway basal cells and matched organoids. Hypomethylated promoters were enriched for genes preferentially expressed in secretory epithelial cells, including BPIFB1, BPIFA2, MSMB and GALNT6. These genes showed little smoking-associated expression difference in basal-cell culture but were upregulated after organoid differentiation, indicating a differentiation-dependent epithelial memory of smoking. In COPD-derived basal cells, promoter methylation changes involved reduced xenobiotic metabolism and enhanced immune- and infection-related programs. Consistently, COPD-derived organoids showed reduced expression of detoxification-associated pathways and increased lysosomal, endocytic and host-defense programs. Current smoking and COPD are associated with persistent methylation-linked regulatory alterations in airway basal cells that become functionally apparent during epithelial differentiation. These findings support a model in which airway basal-cell memory contributes to secretory, inflammatory and host-defense remodeling in chronic airway disease.
-
10. Integrated multiomics reveals a clinically relevant CXCL8-centric protein network in pediatric postinfectious bronchiolitis obliterans.
PMID:日期:2026-08-28Pediatric postinfectious bronchiolitis obliterans (PIBO) is a long-term sequela of severe lower respiratory tract infection. However, the underlying pathogenic mechanisms within the airways remain poorly understood. Bronchoalveolar lavage fluid (BALF) from six children with PIBO and three control children was subjected to transcriptomic, proteomics and untargeted metabolomics analyses. Integrated analysis identified key differentially expressed candidates, among which protein candidates were subsequently validated by ELISAs. Transcriptomic analysis revealed altered pathways in the BALF of children with PIBO, including pathways related to epithelial differentiation, inflammatory responses, and metabolic processes involving amino acids, purines, lipids, and vitamins. Proteomic analysis further revealed epithelial injury, inflammatory activation, tissue remodeling, and metabolic dysregulation in PIBO patients. Protein-protein interaction (PPI) network analysis identified CXCL8 (interleukin-8, IL-8) as the central hub. Integrative transcriptomic-proteomic correlation analysis further revealed that CXCL8 transcript levels were correlated with the greatest number of differentially expressed proteins (DEPs). Subsequent ELISA validation confirmed elevated CXCL8 protein levels in children with PIBO, which were positively correlated with the predicted FEV1%. Furthermore, 54 proteins, including KRT19, OSM, ADAM8, and PADI2, were significantly correlated with CXCL8 expression. These proteins spanned epithelial, inflammatory, remodeling, and metabolic processes, indicating a clinically relevant network. Untargeted metabolomics analysis revealed alterations in purine, cofactors, and amino acid metabolism, with pyridoxine (vitamin B6) as the most significantly altered metabolite. Integrated multiomic analysis revealed widespread correlations between differentially expressed metabolites and proteins. Notably, putative pyridoxine expression was negatively correlated with the expression of CXCL8 and other key inflammatory proteins, which is consistent with the evidence of disrupted vitamin metabolism observed by transcriptomics. In vitro experiments further showed that pyridoxine treatment reduced CXCL8 secretion in small airway epithelial cells. Together, these findings suggest a potential link between vitamin B6 and inflammatory processes in PIBO. Multiomic integration revealed molecular signatures characterized by a CXCL8-centric protein network, a potential disruption of vitamin B6 homeostasis, and altered pathways involved in epithelial differentiation, immunity, and metabolism. These signatures converge on core pathogenic mechanisms within the airway microenvironment, including epithelial injury, inflammatory activation, tissue remodeling, and metabolic dysregulation. Collectively, these findings establish an integrative framework for understanding the pathogenesis of PIBO and highlight potential molecular targets for biomarker discovery and therapeutic intervention.