Experimental Lung Research最新文献

{"title":"Exosomes derived from hypoxic alveolar epithelial cells promote the phenotypic transformation of pulmonary artery smooth muscle cells via the Rap1 pathway","authors":"Guifang Sun, Fangyun Zhao, Yusen Feng, Fei Liu, Xingrui Liu, Yue Jiang, Yating Gao, Jian Hu, Feifei Zhou, Yongju Yang, Zhiqin Du, Caiyan Zhu, Bin Liu","doi":"10.1080/01902148.2024.2398994","DOIUrl":"https://doi.org/10.1080/01902148.2024.2398994","url":null,"abstract":"Background: Hypoxic pulmonary hypertension (HPH) is one of the important pathophysiological changes in chronic pulmonary heart disease. Hypoxia promotes the phenotypic transformation of pulmonary a...","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"13 1","pages":"160-171"},"PeriodicalIF":1.7,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142248682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment with inhaled aerosolised ethanol reduces viral load and potentiates macrophage responses in an established influenza mouse model","authors":"David G. Hancock, Luke Berry, Naomi M. Scott, Kyle T. Mincham, William Ditcham, Alexander N. Larcombe, Barry Clements","doi":"10.1080/01902148.2024.2346320","DOIUrl":"https://doi.org/10.1080/01902148.2024.2346320","url":null,"abstract":"Treatment options for viral lung infections are currently limited. We aimed to explore the safety and efficacy of inhaled ethanol in an influenza-infection mouse model.In a safety and tolerability ...","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140831988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of GBP5 activates autophagy to alleviate inflammatory response in LPS-induced lung injury in mice","authors":"Jialin Li, Kexuan Liu, Wenjuan He, Wencai Zhang, Yongchao Li","doi":"10.1080/01902148.2024.2339269","DOIUrl":"https://doi.org/10.1080/01902148.2024.2339269","url":null,"abstract":"Pulmonary emphysema is a condition that causes damage to the lung tissue over time. GBP5, as part of the guanylate-binding protein family, is dysregulated in mouse pulmonary emphysema. However, the...","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"120 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140624778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential changes in expression of inflammatory mRNA and protein after oleic acid-induced acute lung injury","authors":"Regina Golding, Rudolf K. Braun, Lorenzo Miller, Michael Lasarev, Timothy A. Hacker, Allison C. Rodgers, Ava Staehler, Marlowe W. Eldridge, Awni Al-Subu","doi":"10.1080/01902148.2024.2341099","DOIUrl":"https://doi.org/10.1080/01902148.2024.2341099","url":null,"abstract":"Background: Acute Respiratory Distress syndrome (ARDS) is a clinical syndrome of noncardiac pulmonary edema and inflammation leading to acute respiratory failure. We used the oleic acid infusion pi...","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"44 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140575180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CLCA1 exacerbates lung inflammation via p38 MAPK pathway in acute respiratory distress syndrome","authors":"Xing Lv, Long Zheng, Tianxiang Zhang, Weijia Wang, Yuanyuan Chen, Jing Li, Zhigui Cai, Xingxing Guo, Liqiang Song","doi":"10.1080/01902148.2024.2334262","DOIUrl":"https://doi.org/10.1080/01902148.2024.2334262","url":null,"abstract":"Recent research has revealed that airway epithelial calcium-activated chloride channel-1 (CLCA1) is implicated in the inflammation of multiple human respiratory diseases, but the specific role in a...","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"17 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140602697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-24 regulates obstructive pulmonary disease in rats via S100A8.","authors":"Sha Guo, Qin Liu, Tingting Tan, Xiaoju Chen","doi":"10.1080/01902148.2024.2411852","DOIUrl":"10.1080/01902148.2024.2411852","url":null,"abstract":"<p><strong>Purpose: </strong>Chronic obstructive pulmonary disease (COPD) is a persistent inflammatory disorder characterized by minor airway inflammation and emphysema involving various cell types and cytokines. MicroRNAs (miRNAs) have emerged as critical regulators in the pathogenesis of lung diseases. This study investigates the impact of microRNA-24 (miR-24) on airway inflammatory responses in a rat model of COPD.</p><p><strong>Materials and methods: </strong>The model was established by combining cigarette smoke exposure and lipopolysaccharide stimulation, and rat lung tissues were transfected with adeno-associated viruses overexpressing miR-24. Pathological changes in the lung were assessed using hematoxylin and eosin staining. Levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-6, and interleukin-8, were measured using enzyme-linked immunosorbent assay. Expression of miR-24 and S100A8 was detected through quantitative reverse transcription PCR, while protein levels of S100A8, Toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 (MyD88) were assessed using western blotting. Bioinformatics analysis and dual-luciferase reporter assay were performed to determine the relationship between S100A8 and miR-24.</p><p><strong>Results: </strong>The results demonstrated the downregulation of miR-24 in rats with COPD, and its overexpression resulted in a significant decrease in S1008 mRNA levels. Additionally, the protein level of S100A8 was significantly increased in the lung tissues of COPD rats. The upregulation of miR-24, however, not only inhibited the protein expression of S100A8, TLR4, and MyD88 in lung tissues but also reduced the release of pro-inflammatory cytokines in the plasma and bronchoalveolar lavage fluid, thereby attenuating inflammatory responses and pathological injuries in the lung.</p><p><strong>Conclusions: </strong>Our data suggest that miR-24 attenuates airway inflammatory responses in COPD by inhibiting the TLR4/MyD88 pathway <i>via</i> targeting S100A8.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"50 1","pages":"172-183"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms underlying the roles of leukocytes in the progression of cystic fibrosis.","authors":"Patrick F Asare, Minnu Jayapal, Andrew Tai, Suzanne Maiolo, Sally Chapman, Judith Morton, Emily Hopkins, Paul N Reynolds, Sandra Hodge, Hai Bac Tran","doi":"10.1080/01902148.2024.2424201","DOIUrl":"10.1080/01902148.2024.2424201","url":null,"abstract":"<p><p>Recent advances in cystic fibrosis (CF) treatments have led to improved survival, with life expectancy for Australians living with CF at 57yo. As life expectancy improves, long-term cardiovascular disease risk factors (as for the general population) will become an issue in these patients. We hypothesized that increased leukocyte expression of vasoconstriction and pro-fibrotic mediators may contribute to CF severity in adults with CF. We recruited 13 adult and 24 pediatric healthy controls, and 53 adults and 9 children living with CF. Leukocyte expression/release of endothelin-1 (ET1) and members of the TGF-β/Smad signaling were measured by multifluorescence quantitative confocal microscopy, Western blotting, ELISA, and real-time quantitative polymerase chain reaction. The association between plasma ET1 levels and lung function was assessed. Leukocytes from adults living with CF expressed higher ET1 levels (<i>p</i> = 0.0033), and TGF-β (<i>p</i> = 0.0031); the phosphorylation ratio increased for Smad2/3 (<i>p</i> = 0.0136) but decreased for Smad1/5/8 (<i>p</i> = 0.0007), vs. control subjects. Plasma ET1 levels were significantly increased in adults with CF with FEV₁<50% (<i>p</i> = 0.002) vs. controls, and adults with CF with normal lung function. The release of ET1 in adult plasma inversely correlated with CF severity (-0.609, <i>p</i> = 0.046). Our data indicates that upregulated ET1 and TGF-β/Smad signaling in leukocytes may contribute to CF severity, highlighting the need for further investigations into their impact on the clinical outcomes of people living with CF.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"50 1","pages":"208-220"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cold ischemia time alters cell-type specific senescence leading to loss of cellular integrity in mouse lungs.","authors":"Gagandeep Kaur, Qixin Wang, Ariel Tjitropranoto, Hoshang Unwalla, Irfan Rahman","doi":"10.1080/01902148.2024.2414974","DOIUrl":"10.1080/01902148.2024.2414974","url":null,"abstract":"<p><p><b>Purpose:</b> Ischemia-reperfusion injury (IRI) is a major challenge in lung transplantation often causing graft dysfunction and chronic airway illnesses in recipients. To prevent potential transplant related complications, strict guidelines were put in place to choose viable donor lungs with minimal risk of IRI. These regulations deem most of the donor organs unfit for transplant which then are donated for research to understand the mechanisms of health and diseases in human. However, resected organs that are being transported undergo cold ischemia that can negatively affect the tissue architecture and other cellular functions under study. Thus, it is important to assess how cold ischemia time (CIT) affects the physiological mechanism. In this respect, we are interested in studying how CIT affects cellular senescence in normal aging and various pulmonary pathologies. We thus hypothesized that prolonged CIT exhibits cell-type specific changes in lung cellular senescence in mice. <b>Methods:</b> Lung lobes from C57BL/6J (<i>n</i> = 5-8) mice were harvested and stored in UW Belzer cold storage solution for 0, 4-, 9-, 12-, 24-, and 48-h CIT. Lung cellular senescence was determined using fluorescence (C₁₂FdG) assay and co-immunolabelling was performed to identify changes in individual cell types. <b>Results:</b> We found a rapid decline in the overall lung cellular senescence after 4-h of CIT in our study. Co-immunolabelling revealed the endothelial cells to be most affected by cold ischemia, demonstrating significant decrease in the endothelial cell senescence immediately after harvest. Annexin V-PI staining further revealed a prominent increase in the number of necrotic cells at 4-h CIT, thus suggesting that most of the cells undergo cell death within a few hours of cold ischemic injury. <b>Conclusions:</b> We thus concluded that CIT significantly lowers the cellular senescence in lung tissues and must be considered as a confounding factor for mechanistic studies in the future.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"50 1","pages":"184-198"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11513191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin alleviates lung ischemia-reperfusion injury in a rat lung transplantation model.","authors":"Huizhi Yu, Jing Wang, Mingzhao Liu, Chunlan Hu, Jiaojiao Sun, Bo Xu, Shunmei Lu, Dongxiao Huang, Qingfeng Pang, Chunxiao Hu","doi":"10.1080/01902148.2023.2301615","DOIUrl":"10.1080/01902148.2023.2301615","url":null,"abstract":"<p><p><b>Background:</b> Lung ischemia-reperfusion injury (LIRI) is among the complications observed after lung transplantation and is associated with morbidity and mortality. Preconditioning of the donor lung before organ retrieval may improve organ quality after transplantation. We investigated whether preconditioning with metformin (Met) ameliorates LIRI after lung transplantation. <b>Methods:</b> Twenty Lewis rats were randomly divided into the sham, LIRI, and Met groups. The rats in the LIRI and Met groups received saline and Met, respectively, <i>via</i> oral gavage. Subsequently, a donor lung was harvested and kept in cold storage for 8 h. The LIRI and Met groups then underwent left lung transplantation. After 2 h of reperfusion, serum and transplanted lung tissues were examined. <b>Results:</b> The partial pressure of oxygen (PaO₂) was greater in the Met group than in the LIRI group. In the Met group, wet-to-dry (W/D) weight ratios, inflammatory factor levels, oxidative stress levels and apoptosis levels were notably decreased. <b>Conclusions:</b> Met protects against ischemia-reperfusion injury after lung transplantation in rats, and its therapeutic effect is associated with its anti-inflammatory, antioxidative, and antiapoptotic properties.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"50 1","pages":"15-24"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139691593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leucine rich α2 glycoprotein 1 derived from malignant pleural mesothelioma cells facilitates macrophage M2 phenotypes.","authors":"Dandan Wang, Wenjing Pei, Yanfei Liu, Rongliang Mo, Xinru Li, Wenhui Gu, Yi Su, Jing Ye, Jiegou Xu, Dahai Zhao","doi":"10.1080/01902148.2024.2380988","DOIUrl":"10.1080/01902148.2024.2380988","url":null,"abstract":"<p><p><b>Background:</b> Macrophages constitute the main part of infiltrating immune cells in Malignant pleural mesothelioma (MPM) and abnormally high ratios of M2 macrophages are present in both pleural effusion and tissue samples of MPM patients. Whether MPM cells affect formation of M2 macrophages is poorly understood. In this study, we focused on identification of MPM-cells-derived soluble factors with M2-promoting effects. <b>Methods:</b> Media of malignant pleural mesothelioma cells were collected and soluble factors affecting macrophages were analyzed by mass spectrometry. TGF-β receptor inhibitor SB431542 was used as the entry point to explore the downstream mechanism of action by qRT-PCR, WB and immunofluorescence. <b>Results:</b> The serum-free culture media collected from the human MPM cells Meso1 and Meso2 significantly enhanced expression of the M2 signature molecules including IL-10, TGF-β and CD206 in the human macrophages THP-1, while the culture medium of the human MPM cells H2452 did not show such M2-promoting effects. Analysis of proteins by mass spectrometry and ELISA suggested that Leucine rich α2 glycoprotein 1(LRG1) was a potential candidate. LRG1 time- and dose-dependently increased expression of the M2 signature molecules, confirming its M2-promoting effects. Furthermore, LRG1's M2-promoting effects were reduced by the TGF-β receptor inhibitor SB431542, and LRG1 increased phosphorylation of Smad2, indicating that M2-promoting effects of LRG1 were <i>via</i> the TGF-β receptor/Smad2 signaling pathway. <b>Conclusions:</b> Our results provide a potential M2-promoting new member, LRG1, which contributes to the immune escape of MPM via the TGF-β receptor/Smad2 signaling pathway.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"50 1","pages":"136-145"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}