Experimental Lung Research最新文献_第5页

The multiphasic TNF-α-induced compromise of Calu-3 airway epithelial barrier function. 多相TNF-α-诱导Calu-3气道上皮屏障功能受损。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 DOI: 10.1080/01902148.2023.2193637

Katherine M DiGuilio, Elizabeth Rybakovsky, Yoongyeong Baek, Mary Carmen Valenzano, James M Mullin

{"title":"The multiphasic TNF-α-induced compromise of Calu-3 airway epithelial barrier function.","authors":"Katherine M DiGuilio, Elizabeth Rybakovsky, Yoongyeong Baek, Mary Carmen Valenzano, James M Mullin","doi":"10.1080/01902148.2023.2193637","DOIUrl":"https://doi.org/10.1080/01902148.2023.2193637","url":null,"abstract":"Purpose: Airway epithelial barrier leak and the involvement of proinflammatory cytokines play a key role in a variety of diseases. This study evaluates barrier compromise by the inflammatory mediator Tumor Necrosis Factor-α (TNF-α) in the human airway epithelial Calu-3 model. Methods: We examined the effects of TNF-α on barrier function in Calu-3 cell layers using Transepithelial Electrical Resistance (TER) and transepithelial diffusion of radiolabeled probe molecules. Western immunoblot analyses of tight junctional (TJ) proteins in detergent soluble fractions were performed. Results: TNF-α dramatically reduced TER and increased paracellular permeability of both 14C-D-mannitol and the larger 5 kDa probe, 14C-inulin. A time course of the effects shows two separate actions on barrier function. An initial compromise of barrier function occurs 2-4 hours after TNF-α exposure, followed by complete recovery of barrier function by 24 hrs. Beginning 48 hrs. post-exposure, a second more sustained barrier compromise ensues, in which leakiness persists through 144 hrs. There were no changes in TJ proteins observed at 3 hrs. post exposure, but significant increases in claudins-2, -3, -4, and -5, as well as a decrease in occludin were seen at 72 hrs. post TNF-α exposure. Both the 2-4 hr. and the 72 hr. TNF-α induced leaks are shown to be mediated by the ERK signaling pathway. Conclusion: TNF-α induced a multiphasic transepithelial leak in Calu-3 cell layers that was shown to be ERK mediated, as well as involve changes in the TJ complex. The micronutrients, retinoic acid and calcitriol, were effective at reducing this barrier compromise caused by TNF-α. The significance of these results for airway disease and for COVID-19 specifically are discussed.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"72-85"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9658606","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: 1

Comparison of hypoxia-induced pulmonary hypertension rat models caused by different hypoxia protocols. 不同缺氧方案致肺动脉高压大鼠模型的比较。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 DOI: 10.1080/01902148.2022.2148016

Gexiang Cai, Yaxin Zhang, Xinghong Wang, Shini Li, Yushan Cheng, Xiaoying Huang

{"title":"Comparison of hypoxia-induced pulmonary hypertension rat models caused by different hypoxia protocols.","authors":"Gexiang Cai, Yaxin Zhang, Xinghong Wang, Shini Li, Yushan Cheng, Xiaoying Huang","doi":"10.1080/01902148.2022.2148016","DOIUrl":"https://doi.org/10.1080/01902148.2022.2148016","url":null,"abstract":"Background and aim: Pulmonary hypertension (PH) is a serious and even fatal disorder with limited treatment strategies. The hypoxia-induced pulmonary hypertension (HPH) rat model is commonly used in this field. While the HPH rat model has strong predictability and repeatability, the model is a chronic model, making it time-consuming, costly, and complicated and limiting the progress of the experiments. Currently, there is no uniform international standard for the HPH model. Our study aimed to find a relatively effective and efficient HPH modeling protocol. Methods: We established HPH rat models with different total hypoxia periods and different daily hypoxia times, and assessed different hypoxia modeling modes in multiple dimensions, such as haemodynamics, right ventricular (RV) hypertrophy, pulmonary arterial remodeling, muscularization, inflammation, and collagen deposition. Results: Longer daily hypoxia time resulted in higher mean pulmonary arterial pressure (mPAP)/right ventricular systolic pressure (RVSP) and more obvious RV hypertrophy, as well as more severe pulmonary arterial remodeling and muscularization, regardless of the total period of hypoxia (3- or 4-week). Moreover, pulmonary perivascular macrophages and collagen deposition showed daily hypoxia time-dependent increases, both in 3- and 4-week hypoxia groups. Conclusion: Our findings showed that the 3-week continuous hypoxia mode was a relatively efficient way to reduce the time needed to induce significant disease phenotypes, which offered methodological evidence for future studies in building HPH models.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732421","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

HIF and ER stress are involved in TGFβ1-mediated wound closure of alveolar epithelial cells. HIF和内质网应激参与tgf β1介导的肺泡上皮细胞伤口闭合。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 DOI: 10.1080/01902148.2023.2183996

Eva Delbrel, Nicolas Voituron, Emilie Boncoeur

{"title":"HIF and ER stress are involved in TGFβ1-mediated wound closure of alveolar epithelial cells.","authors":"Eva Delbrel, Nicolas Voituron, Emilie Boncoeur","doi":"10.1080/01902148.2023.2183996","DOIUrl":"https://doi.org/10.1080/01902148.2023.2183996","url":null,"abstract":"Purpose: Alveolar epithelium dysfunction is associated with a very large spectrum of disease and an abnormal repair capacity of the airway epithelium has been proposed to explain the pathogenesis of Idiopathic Pulmonary Fibrosis (IPF). Following epithelium insult, the damaged cells will activate pathways implicated in the repair process, including proliferation and acquisition of migratory capacities to cover the denuded basement membrane. Induction of Endoplasmic Reticulum stress may be implicated in this process. Interestingly, ER stress excessive activation has been proposed as a central event associated with aberrant repair process and cellular dysfunction observed in IPF. Methods: We study by wound healing assay the molecular targets associated with Alveolar Epithelial Cells (AEC) repair. Results: We demonstrate that the wound recovery of AEC is associated with TGF-β1 signaling and increased transcriptional activity of ER stress and HIF-dependent genes. We further demonstrated that inhibition of TGF-β1 signaling, CHOP expression or HIF-1 expression, limits AECs wound closure. Conclusion: the use of pharmacological drugs targeting the ER/HIF-1 axis could be an attractive approach to limit AEC dysregulation in pathological condition, and confirmed a critical role of theses factor in response to alveolar injury.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"63-71"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9952979","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

House dust mite-induced endoplasmic reticulum stress mediates MUC5AC hypersecretion via TBK1 in airway epithelium. 屋尘螨诱导的内质网应激通过TBK1介导气道上皮MUC5AC的高分泌。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 DOI: 10.1080/01902148.2023.2170494

Jun Deng, Hongmei Tang, Yun Zhang, Xiefang Yuan, Ning Ma, Hang Hu, Xiaoyun Wang, Chunfeng Liu, Guofeng Xu, Yuejiao Li, Songping Wang, Linlin Guo, Xing Wang

{"title":"House dust mite-induced endoplasmic reticulum stress mediates MUC5AC hypersecretion via TBK1 in airway epithelium.","authors":"Jun Deng, Hongmei Tang, Yun Zhang, Xiefang Yuan, Ning Ma, Hang Hu, Xiaoyun Wang, Chunfeng Liu, Guofeng Xu, Yuejiao Li, Songping Wang, Linlin Guo, Xing Wang","doi":"10.1080/01902148.2023.2170494","DOIUrl":"https://doi.org/10.1080/01902148.2023.2170494","url":null,"abstract":"Purpose: Endoplasmic reticulum (ER) stress regulates mucus hypersecretion, and may activate downstream factors via TBK1 signaling to induce gene expression. However, it remains unclear whether ER stress promotes airway mucus secretion through the TBK1 pathway. We aimed to investigate the role of the TBK1 pathway in the regulation of MUC5AC expression in a mouse model of house dust mite (HDM)-induced allergic asthma. Materials and Methods: Mice with HDM-induced asthma and human bronchial epithelial BEAS-2B cells were treated with amlexanox, an anti-allergy drug (25 μM), or 4-PBA (10 mM). Tissue and cell samples were collected. Tissue samples were stained with hematoxylin and eosin (H&E) or periodic acid Schiff (PAS) to evaluate pathology. Protein expression was analyzed by western blotting and immunofluorescence. Results: Mice exposed to HDM presented ER stress and hypersecretion of mucus Muc5ac from airway epithelial cells (p < 0.001). Similar results were observed in BEAS-2B cells following exposure to HDM. Both in vivo and in vitro studies revealed that HDM-induced ER stress induced MUC5AC overexpression via TBK1 signaling. Amlexanox and 4-PBA markedly reduced mucus production and weakened the TBK1 signal, which mediates MUC5AC hypersecretion. Conclusion: TBK1 plays a pivotal role in HDM-induced ER stress, leading to overproduction of MUC5AC in the asthmatic airway epithelium. The overproduction of MUC5AC can be significantly decreased by inhibiting TBK1 or ER stress using 4-PBA. These findings highlight potential target-specific therapies for patients with chronic allergic asthma.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"49-62"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9971416","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: 3

Rapamycin attenuates pyroptosis by suppressing mTOR phosphorylation and promoting autophagy in LPS-induced bronchopulmonary dysplasia. 雷帕霉素通过抑制mTOR磷酸化和促进LPS诱导的支气管肺发育不良中的自噬来减轻焦下垂。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 Epub Date: 2023-10-24 DOI: 10.1080/01902148.2023.2266236

Feng Zhang, Minrong Wang, Zhongni Li, Jiehong Deng, Yang Fan, Zhixian Gou, Yue Zhou, Li Huang, Liqun Lu

{"title":"Rapamycin attenuates pyroptosis by suppressing mTOR phosphorylation and promoting autophagy in LPS-induced bronchopulmonary dysplasia.","authors":"Feng Zhang, Minrong Wang, Zhongni Li, Jiehong Deng, Yang Fan, Zhixian Gou, Yue Zhou, Li Huang, Liqun Lu","doi":"10.1080/01902148.2023.2266236","DOIUrl":"10.1080/01902148.2023.2266236","url":null,"abstract":"Purpose/aim: Bronchopulmonary dysplasia (BPD) is associated with poor survival in preterm infants. Intrauterine infection can aggravate the degree of obstruction of alveolar development in premature infants; however, the pathogenic mechanism remains unclear. In this study, we sought to determine whether pyroptosis could be inhibited by downregulating mammalian target of rapamycin (mTOR) activation and inducing autophagy in BPD-affected lung tissue.Materials and methods: We established a neonatal rat model of BPD induced by intrauterine infection via intraperitoneally injecting pregnant rats with lipopolysaccharide (LPS). Subsequently, mTOR levels and pyroptosis were evaluated using immunohistochemistry, immunofluorescence, TUNEL staining, and western blotting. The Shapiro-Wilk test was employed to assess the normality of the experimental data. Unpaired t-tests were used to compare the means between two groups, and comparisons between multiple groups were performed using analysis of variance.Results: Pyroptosis of lung epithelial cells increased in BPD lung tissues. After administering an mTOR phosphorylation inhibitor (rapamycin) to neonatal rats with BPD, the level of autophagy increased, while the expression of autophagy cargo adaptors, LC3 and p62, did not differ. Following rapamycin treatment, NLRP3, Pro-caspase-1, caspase-1, pro-IL-1β, IL-1β, IL-18/Pro-IL-18, N-GSDMD/GSDMD, Pro-caspase-11, and caspase-11 were negatively regulated in BPD lung tissues. The opposite results were observed after treatment with the autophagy inhibitor MHY1485, showing an increase in pyroptosis and a significant decrease in the number of alveoli in BPD.Conclusions: Rapamycin reduces pyroptosis in neonatal rats with LPS-induced BPD by inhibiting mTOR phosphorylation and inducing autophagy; hence, it may represent a potential therapeutic for treating BPD.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"178-192"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49689470","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

Inhibition of cGAS aggravated the host inflammatory response to Aspergillus fumigatus. 抑制 cGAS 会加重宿主对曲霉菌的炎症反应。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2023-01-01 Epub Date: 2023-05-16 DOI: 10.1080/01902148.2023.2211663

Mei Peng, Xiujun Li, Xiaobing Zhang, Li Peng

{"title":"Inhibition of cGAS aggravated the host inflammatory response to Aspergillus fumigatus.","authors":"Mei Peng, Xiujun Li, Xiaobing Zhang, Li Peng","doi":"10.1080/01902148.2023.2211663","DOIUrl":"10.1080/01902148.2023.2211663","url":null,"abstract":"Backgroud: Aspergillus fumigatus (A. fumigatus) is a clinically important fungal pathogen. Invasive pulmonary aspergillosis (IPA) is the main fungal infection with increased morbidity and mortality in immunocompromised populations, although treatments are available. An innate DNA sensor known as cyclic GMP-AMP Synthase (cGAS) has recently been discovered that senses invading pathogens and has a significant impact on innate immunity. It can activate the cGAS-STING signaling pathway to stimulate downstream signals. But it is still unclear what role it plays in IPA's pathogenesis.Methods: An investigation into the infection of A. fumigatus was conducted by inhibiting cGAS activity in vivo and in vitro using siRNA and RU.521(an inhibitor of cGAS).Results: We discovered that suppressing cGAS increased the host's susceptibility to A. fumigatus and harmed those with infections by enhancing pulmonary tissue damage and edema, as well as decreasing fungal clearance. Furthermore, our findings show that inhibiting or silencing cGAS can exacerbate the inflammatory response in IPA mouse models and human bronchi epithelial cells (HBECs) treated with A. fumigatus by upregulating the production of inflammatory genes with non-type 1 interferon.Conclusion: Based on our analysis, we conclude that activating cGAS might increase host resistance to A. fumigatus, protect against pulmonary illnesses brought on by A. fumigatus and that exploring the cGAS-STING signaling pathway is beneficial not only for the immunological investigation of IPA but also may be a potential therapeutic objective.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":" ","pages":"86-100"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9463465","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

Prevention of submicron aerosolized particle dispersion: evaluation of an aerosol box using a pediatric simulation model. 预防亚微米雾化颗粒分散:使用儿科模拟模型评估气溶胶盒。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2022-11-01 DOI: 10.1080/01902148.2022.2135795

Laurence Tabone, Dominic Rivest, Arielle Levy, Michael Buyck, Philippe Jouvet, Carl-Eric Aubin, Tine François, Etienne Robert, Florent Baudin

{"title":"Prevention of submicron aerosolized particle dispersion: evaluation of an aerosol box using a pediatric simulation model.","authors":"Laurence Tabone, Dominic Rivest, Arielle Levy, Michael Buyck, Philippe Jouvet, Carl-Eric Aubin, Tine François, Etienne Robert, Florent Baudin","doi":"10.1080/01902148.2022.2135795","DOIUrl":"https://doi.org/10.1080/01902148.2022.2135795","url":null,"abstract":"Background and Aim: The SplashGuard CG (SG) is a barrier enclosure developed to protect healthcare workers from SARS-CoV-2 transmission during aerosol-generating procedures. Our objective was to evaluate the protection provided by the SG against aerosolized particles (AP), using a pediatric simulation model of spontaneous ventilation (SV) and noninvasive ventilation (NIV). Methods: An aerosol generator was connected to the airways of a pediatric high-fidelity manikin with a breathing simulator. AP concentrations were measured both in SV and NIV in the following conditions: with and without SG, inside and outside the SG, with and without suction applied to the device. Results: In the SV simulated setting, AP peaks were lower with SG: 0.1 × 105 particles/L compared to without: 1.6 × 105, only when the ports were closed and suction applied. In the NIV simulated setting, AP peaks outside the SG were lower than without SG (20.5 × 105 particles/L), whatever the situation, without suction (14.4 × 105particles/L), with suction and ports open or closed: 10.3 and 0.7 × 105 particles/L. In SV and NIV simulated settings, the AP peaks measured within the SG were much higher than the AP peaks measured without SG, even when suction was applied to the device. Conclusions: The SG seems to decrease peak AP exposure in the 2 ventilation contexts, but only with closed port and suction in SV. However, high concentrations of AP remain inside even with suction and SG should be used cautiously.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"266-274"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10440548","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

Proteomic global proteins analysis in blast lung injury reveals the altered characteristics of crucial proteins in response to oxidative stress, oxidation-reduction process and lipid metabolic process. 蛋白质组学分析揭示了肺损伤中氧化应激、氧化还原过程和脂质代谢过程中关键蛋白的改变特征。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2022-11-01 DOI: 10.1080/01902148.2022.2143596

Peifang Cong, Changci Tong, Shun Mao, Xiuyun Shi, Ying Liu, Lin Shi, Hongxu Jin, Yunen Liu, Mingxiao Hou

{"title":"Proteomic global proteins analysis in blast lung injury reveals the altered characteristics of crucial proteins in response to oxidative stress, oxidation-reduction process and lipid metabolic process.","authors":"Peifang Cong, Changci Tong, Shun Mao, Xiuyun Shi, Ying Liu, Lin Shi, Hongxu Jin, Yunen Liu, Mingxiao Hou","doi":"10.1080/01902148.2022.2143596","DOIUrl":"https://doi.org/10.1080/01902148.2022.2143596","url":null,"abstract":"Background: Blast lung injury (BLI) is the most common fatal blast injury induced by overpressure wave in the events of terrorist attack, gas and underground explosion. Our previous work revealed the characteristics of inflammationrelated key proteins involved in BLI, including those regulating inflammatory response, leukocyte transendothelial migration, phagocytosis, and immune process. However, the molecular characteristics of oxidative-related proteins in BLI ar still lacking. Methods: In this study, protein expression profiling of the blast lungs obtained by tandem mass tag (TMT) spectrometry quantitative proteomics were re-analyzed to identify the characteristics of oxidative-related key proteins. Forty-eight male C57BL/6 mice were randomly divided into six groups: control, 12 h, 24 h, 48 h, 72 h and 1 w after blast exposure. The differential protein expression was identified by bioinformatics analysis and verified by western blotting. Results: The results demonstrated that thoracic blast exposure induced reactive oxygen species generation and lipid peroxidation in the lungs. Analysis of global proteins and oxidative-related proteomes showed that 62, 59, 73, 69, 27 proteins (accounted for 204 distinct proteins) were identified to be associated with oxidative stress at 12 h, 24 h, 48 h, 72 h, and 1 week after blast exposure, respectively. These 204 distinct proteins were mainly enriched in response to oxidative stress, oxidation-reduction process and lipid metabolic process. We also validated these results by western blotting. Conclusions: These findings provided new perspectives on blast-induced oxidative injury in lung, which may potentially benefit the development of future treatment of BLI.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"275-290"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10441092","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

Effect of mycobacterial proteins that target mitochondria on the alveolar macrophages activation during Mycobacterium tuberculosis infection. 靶向线粒体的分枝杆菌蛋白对结核分枝杆菌感染期间肺泡巨噬细胞活化的影响。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2022-11-01 DOI: 10.1080/01902148.2022.2120649

Iris Selene Paredes-González, Omar Emiliano Aparicio-Trejo, Octavio Ramos-Espinosa, Manuel Othoniel López-Torres, Milena Maya-Hoyos, Monserrat Mendoza-Trujillo, Alejandra Barrera-Rosales, Dulce Mata-Espinosa, Juan Carlos León-Contreras, José Pedraza-Chaverri, Clara Espitia, Rogelio Hernández-Pando

{"title":"Effect of mycobacterial proteins that target mitochondria on the alveolar macrophages activation during Mycobacterium tuberculosis infection.","authors":"Iris Selene Paredes-González, Omar Emiliano Aparicio-Trejo, Octavio Ramos-Espinosa, Manuel Othoniel López-Torres, Milena Maya-Hoyos, Monserrat Mendoza-Trujillo, Alejandra Barrera-Rosales, Dulce Mata-Espinosa, Juan Carlos León-Contreras, José Pedraza-Chaverri, Clara Espitia, Rogelio Hernández-Pando","doi":"10.1080/01902148.2022.2120649","DOIUrl":"https://doi.org/10.1080/01902148.2022.2120649","url":null,"abstract":"Purpose of the study: During the early and progressive (late) stages of murine experimental pulmonary tuberculosis, the differential activation of macrophages contributes to disease development by controlling bacterial growth and immune regulation. Mycobacterial proteins P27 and PE_PGRS33 can target the mitochondria of macrophages. This study aims to evaluate the effect of both proteins on macrophage activation during mycobacterial infection. Materials and methods: We assess both proteins for mitochondrial oxygen consumption, and morphological changes, as well as bactericide activity, production of metabolites, cytokines, and activation markers in infected MQs. The cell line MH-S was used for all the experiments. Results: We show that P27 and PE_PGRS33 proteins modified mitochondrial dynamics, oxygen consumption, bacilli growth, cytokine production, and some genes that contribute to macrophage alternative activation and mycobacterial intracellular survival. Conclusions: Our findings showed that these bacterial proteins partially contribute to promoting M2 differentiation by altering mitochondrial metabolic activity.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"251-265"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10431874","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: 1

Changes in lung sialidases in male and female mice after bleomycin aspiration. 博来霉素吸入后雌雄小鼠肺唾液酸酶的变化。

IF 1.7 4区医学

Experimental Lung Research Pub Date : 2022-11-01 Epub Date: 2022-11-16 DOI: 10.1080/01902148.2022.2144548

Darrell Pilling, Kyle Sahlberg, Wensheng Chen, Richard H Gomer

{"title":"Changes in lung sialidases in male and female mice after bleomycin aspiration.","authors":"Darrell Pilling, Kyle Sahlberg, Wensheng Chen, Richard H Gomer","doi":"10.1080/01902148.2022.2144548","DOIUrl":"10.1080/01902148.2022.2144548","url":null,"abstract":"Aim of the study: Sialidases, also called neuraminidases, are enzymes that cleave terminal sialic acids from glycoconjugates. In humans and mice, lung fibrosis is associated with desialylation of glycoconjugates and upregulation of sialidases. There are four mammalian sialidases, and it is unclear when the four mammalian sialidases are elevated over the course of inflammatory and fibrotic responses, whether tissue resident and inflammatory cells express different sialidases, and if sialidases are differentially expressed in male and females. Materials and Methods: To determine the time course of sialidase expression and the identity of sialidase expressing cells, we used the bleomycin model of pulmonary fibrosis in mice to examine levels of sialidases during inflammation (days 3 - 10) and fibrosis (days 10 - 21). Results: Bleomycin aspiration increased sialidase NEU1 at days 14 and 21 in male mice and day 10 in female mice. NEU2 levels increased at day 7 in male and day 10 in female mice. NEU3 appears to have a biphasic response in male mice with increased levels at day 7 and then at days 14 and 21, whereas in female mice NEU3 levels increased over 21 days. In control mice, the sialidases were mainly expressed by EpCAM positive epithelial cells, but after bleomycin, epithelial cells, CD45 positive immune cells, and alveolar cells expressed NEU1, NEU2, and NEU3. Sialidase expression was higher in male compared to female mice. There was little expression of NEU4 in murine lung tissue. Conclusions: These results suggest that sialidases are dynamically expressed following bleomycin, that sialidases are differentially expressed in male and females, and that of the four sialidases only NEU3 upregulation is associated with fibrosis in both male and female mice.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"291-304"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10084762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9647972","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}

引用次数: 1