Experimental Lung Research最新文献

Exosomes derived from hypoxic alveolar epithelial cells promote the phenotypic transformation of pulmonary artery smooth muscle cells via the Rap1 pathway 来自缺氧肺泡上皮细胞的外泌体通过 Rap1 途径促进肺动脉平滑肌细胞的表型转化

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-09-17 DOI: 10.1080/01902148.2024.2398994

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

引用次数: 0

Treatment with inhaled aerosolised ethanol reduces viral load and potentiates macrophage responses in an established influenza mouse model 在已建立的流感小鼠模型中，吸入气溶胶乙醇可降低病毒载量并增强巨噬细胞的反应能力

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-04-29 DOI: 10.1080/01902148.2024.2346320

David G. Hancock, Luke Berry, Naomi M. Scott, Kyle T. Mincham, William Ditcham, Alexander N. Larcombe, Barry Clements

引用次数: 0

Inhibition of GBP5 activates autophagy to alleviate inflammatory response in LPS-induced lung injury in mice 抑制 GBP5 可激活自噬，减轻 LPS 诱导的小鼠肺损伤的炎症反应

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-04-20 DOI: 10.1080/01902148.2024.2339269

Jialin Li, Kexuan Liu, Wenjuan He, Wencai Zhang, Yongchao Li

引用次数: 0

Differential changes in expression of inflammatory mRNA and protein after oleic acid-induced acute lung injury 油酸诱导急性肺损伤后炎症 mRNA 和蛋白质表达的差异变化

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-04-16 DOI: 10.1080/01902148.2024.2341099

Regina Golding, Rudolf K. Braun, Lorenzo Miller, Michael Lasarev, Timothy A. Hacker, Allison C. Rodgers, Ava Staehler, Marlowe W. Eldridge, Awni Al-Subu

引用次数: 0

CLCA1 exacerbates lung inflammation via p38 MAPK pathway in acute respiratory distress syndrome CLCA1 在急性呼吸窘迫综合征中通过 p38 MAPK 通路加剧肺部炎症

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-04-10 DOI: 10.1080/01902148.2024.2334262

Xing Lv, Long Zheng, Tianxiang Zhang, Weijia Wang, Yuanyuan Chen, Jing Li, Zhigui Cai, Xingxing Guo, Liqiang Song

引用次数: 0

Metformin alleviates lung ischemia-reperfusion injury in a rat lung transplantation model. 二甲双胍减轻大鼠肺移植模型中的肺缺血再灌注损伤

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-01-01 Epub Date: 2024-02-05 DOI: 10.1080/01902148.2023.2301615

Huizhi Yu, Jing Wang, Mingzhao Liu, Chunlan Hu, Jiaojiao Sun, Bo Xu, Shunmei Lu, Dongxiao Huang, Qingfeng Pang, Chunxiao Hu

{"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":"Background: 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. Methods: 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, via 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. Results: 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. Conclusions: 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.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":null,"pages":null},"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}

引用次数: 0

Leucine rich α2 glycoprotein 1 derived from malignant pleural mesothelioma cells facilitates macrophage M2 phenotypes. 从恶性胸膜间皮瘤细胞中提取的富亮氨酸α2糖蛋白1可促进巨噬细胞M2表型的形成。

IF 1.5 4区医学

Experimental Lung Research Pub Date : 2024-01-01 Epub Date: 2024-07-21 DOI: 10.1080/01902148.2024.2380988

Dandan Wang, Wenjing Pei, Yanfei Liu, Rongliang Mo, Xinru Li, Wenhui Gu, Yi Su, Jing Ye, Jiegou Xu, Dahai Zhao

{"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":"Background: 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. Methods: 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. Results: 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 via the TGF-β receptor/Smad2 signaling pathway. Conclusions: 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.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":null,"pages":null},"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}

引用次数: 0

Protective effect of liver X receptor on cigarette smoke and lipopolysaccharide induced airway inflammation and emphysema in mice. 肝 X 受体对香烟烟雾和脂多糖诱发的小鼠气道炎症和肺气肿的保护作用

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-01-01 Epub Date: 2024-03-21 DOI: 10.1080/01902148.2024.2329436

Fenfang Yu, Lin Gao, Ke Xu, Xiaobing Yang, Junran Zhang, Yu Tang, Zhifei Ma, Wei Gu, Bining Wu, Ying Shi

{"title":"Protective effect of liver X receptor on cigarette smoke and lipopolysaccharide induced airway inflammation and emphysema in mice.","authors":"Fenfang Yu, Lin Gao, Ke Xu, Xiaobing Yang, Junran Zhang, Yu Tang, Zhifei Ma, Wei Gu, Bining Wu, Ying Shi","doi":"10.1080/01902148.2024.2329436","DOIUrl":"10.1080/01902148.2024.2329436","url":null,"abstract":"Objective: The aim of this study is to assess the impact of Liver X receptors (LXRs) on airway inflammation, airway remodeling, and lipid deposition induced by cigarette smoke and lipopolysaccharide (LPS) exposure in the lung.Methods: Wild mice and LXR-deficient mice were exposed to cigarette smoke and LPS to induce airway inflammation and remodeling. In addition, some wild mice received intraperitoneal treatment with the LXR agonist GW3965 before exposure to cigarette smoke and LPS. Lung tissue and bronchoalveolar lavage fluid were collected to evaluate airway inflammation, airway remodeling and lipid deposition.Results: Exposure to cigarette smoke and LPS resulted in airway inflammation, emphysema and lipid accumulation in wild mice. These mice also exhibited downregulated LXRα and ABCA1 in the lung. Treatment with GW3965 mitigated inflammation, remodeling and lipid deposition, while the deletion of LXRs exacerbated these effects. Furthermore, GW3965 treatment following exposure to cigarette smoke and LPS increased LXRα and ABCA1 expression and attenuated MyD88 expression in wild mice.Conclusion: LXRs demonstrate the potential to mitigate cigarette smoke and LPS- induced airway inflammation, emphysema and lipid disposition in mice.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174159","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}

引用次数: 0

High oxygen exposure's impact on newborn mice: Temporal changes observed via micro-computed tomography. 高氧暴露对新生小鼠的影响：通过微型计算机断层扫描观察到的时间变化

IF 1.5 4区医学

Experimental Lung Research Pub Date : 2024-01-01 Epub Date: 2024-07-08 DOI: 10.1080/01902148.2024.2375099

Himeko Sato, Akie Kato, Hiroyuki Adachi, Kiichi Takahashi, Hirokazu Arai, Masato Ito, Fumihiko Namba, Tsutomu Takahashi

{"title":"High oxygen exposure's impact on newborn mice: Temporal changes observed via micro-computed tomography.","authors":"Himeko Sato, Akie Kato, Hiroyuki Adachi, Kiichi Takahashi, Hirokazu Arai, Masato Ito, Fumihiko Namba, Tsutomu Takahashi","doi":"10.1080/01902148.2024.2375099","DOIUrl":"https://doi.org/10.1080/01902148.2024.2375099","url":null,"abstract":"Introduction: Bronchopulmonary dysplasia (BPD) impacts life expectancy and long-term quality of life. Currently, BPD mouse models exposed to high oxygen are frequently used, but to reevaluate their relevance to human BPD, we attempted an assessment using micro-computed tomography (µCT).Methods: Newborn wildtype male mice underwent either 21% or 95% oxygen exposure for 4 days, followed until 8 wk. Weekly µCT scans and lung histological evaluations were performed independently.Results: Neonatal hyperoxia for 4 days hindered lung development, causing alveolar expansion and simplification. Histologically, during the first postnatal week, the exposed group showed a longer mean linear intercept, enlarged alveolar area, and a decrease in alveolar number, diminishing by week 4. Weekly µCT scans supported these findings, revealing initially lower lung density in newborn mice, increasing with age. However, the high-oxygen group displayed higher lung density initially. This difference diminished over time, with no significant contrast to controls at 3 wk. Although no significant difference in total lung volume was observed at week 1, the high-oxygen group exhibited a decrease by week 2, persisting until 8 wk.Conclusion: This study highlights µCT-detected changes in mice exposed to high oxygen. BPD mouse models might follow a different recovery trajectory than humans, suggesting the need for further optimization.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554455","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}

引用次数: 0

Exosomal miR-223 promotes ARDS by targeting insulin-like growth factor 1 receptor: A cell communication study. 外泌体 miR-223 通过靶向胰岛素样生长因子 1 受体促进 ARDS：细胞通讯研究

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2024-01-01 Epub Date: 2024-03-01 DOI: 10.1080/01902148.2024.2318561

Miaomiao Li, Lilei Zhuang, Tao Jiang, Li Sun

{"title":"Exosomal miR-223 promotes ARDS by targeting insulin-like growth factor 1 receptor: A cell communication study.","authors":"Miaomiao Li, Lilei Zhuang, Tao Jiang, Li Sun","doi":"10.1080/01902148.2024.2318561","DOIUrl":"10.1080/01902148.2024.2318561","url":null,"abstract":"Background: Acute respiratory distress syndrome (ARDS) is a respiratory failure syndrome characterized by hypoxemia and changes in the respiratory system. ARDS is the most common cause of death in COVID-19 deaths was ARDS. In this study, we explored the role of miR-223 in exosomes in ARDS.Methods: Exosomes were purified from the supernatants of macrophages. qPCR was used to detect relative mRNA levels. A luciferase reporter assay was performed to verify the miRNA target genes. Western blotting was used to detect the activation of inflammatory pathways. Flow cytometry was performed to assess apoptosis. An LPS-induced ARDS mouse model was used to assess the function of miR-223 in ARDS.Results: Exosomes secreted by macrophages promoted apoptosis in A549 cells. Macrophages and exosomes contain high levels of miR-223. Exogenous miR-223 can decrease the expression of insulin-like growth factor 1 receptor (IGF-1R) in A549 and promote the apoptosis of A549.Transfection of anti-miR223 antisense nucleotides effectively reduced the level of miR-223 in macrophages and exosomes and eliminated the pro-apoptotic effect of A549. In vivo, LPS stimulation increased inflammatory cell infiltration in the lungs of mice, whereas knockdown of miR-223 in mice resulted in significantly reduced eosinophil infiltration.Conclusions: Macrophages can secrete exosomes containing miR-223 and promote apoptosis by targeting the IGF-1R/Akt/mTOR signaling pathway in A549 cells and mouse models, suggesting that miR-223 is a potential target for treating COVID-19 induced ARDS.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139995973","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}

引用次数: 0