Experimental Lung Research最新文献

{"title":"Effect of mycobacterial proteins that target mitochondria on the alveolar macrophages activation during <i>Mycobacterium tuberculosis</i> infection.","authors":"Iris Selene Paredes-González,&nbsp;Omar Emiliano Aparicio-Trejo,&nbsp;Octavio Ramos-Espinosa,&nbsp;Manuel Othoniel López-Torres,&nbsp;Milena Maya-Hoyos,&nbsp;Monserrat Mendoza-Trujillo,&nbsp;Alejandra Barrera-Rosales,&nbsp;Dulce Mata-Espinosa,&nbsp;Juan Carlos León-Contreras,&nbsp;José Pedraza-Chaverri,&nbsp;Clara Espitia,&nbsp;Rogelio Hernández-Pando","doi":"10.1080/01902148.2022.2120649","DOIUrl":"https://doi.org/10.1080/01902148.2022.2120649","url":null,"abstract":"<p><p><b>Purpose of the study:</b> 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. <b>Materials and methods:</b> 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. <b>Results:</b> 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. <b>Conclusions:</b> Our findings showed that these bacterial proteins partially contribute to promoting M2 differentiation by altering mitochondrial metabolic activity.</p>","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}

{"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":"<p><p><b>Aim of the study:</b> 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. <b>Materials and Methods:</b> 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). <b>Results:</b> 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. <b>Conclusions:</b> 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.</p>","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}

{"title":"Effect of using acoustic flo-tone training device and its smartphone application on enhancing inhalation technique from metered-dose inhaler with spacer in asthmatic children.","authors":"Sara M Tony,&nbsp;Mona A Abdelrahman,&nbsp;Mogeda Abd Elsalam,&nbsp;Mahmoud Sameer Shafik,&nbsp;Mohamed E A Abdelrahim","doi":"10.1080/01902148.2022.2113573","DOIUrl":"https://doi.org/10.1080/01902148.2022.2113573","url":null,"abstract":"<p><p><b>Aim of study:</b> This research study aims to compare between two different counseling approaches; traditional verbal counseling vs. advanced counseling (in which we used the acoustic Flo-tone training device and its smartphone application combined with traditional verbal counseling) to determine the most beneficial counseling approach for asthmatic children who use metered-dose inhaler (MDI) with spacers concerning inhalation duration and inhalation technique mistakes. <b>Methods:</b> A total of 100 asthmatic children (8-18) years old were randomized into two groups (a control group, and an advanced group). Each group included 50 subjects. Every subject received 3 counseling meetings, one each month. Asthmatic children in the control group were trained on inhalation technique from MDI + spacer verbally (traditional counseling), while asthmatic children in advanced group were trained on inhalation technique from MDI + spacer verbally and by advanced counseling (whistling Flo-tone + smartphone application). At each visit mistakes in inhalation technique steps were; detected, corrected, and recorded and the inhalation duration was measured for every child in each group. <b>Results:</b> In both study groups, the total mean number of inhalation technique mistakes decreased significantly (p < 0.05) from visit 2, also the total mean inhalation durations in seconds showed a significant increase (p < 0.05) from visit 2. A significant (p < 0.05) reduction in the total mean number of mistakes and a significant (p < 0.05) increase in total mean inhalation durations were observed from visit 2 in advanced group compared to control group. <b>Conclusion:</b> Combination between traditional verbal and advanced counseling methods resulted in significant (P < 0.05) improvements in the number of inhalation technique mistakes and inhalation durations from MDI with spacer in children compared to using traditional verbal counseling alone.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 7-8","pages":"224-238"},"PeriodicalIF":1.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40649108","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":"BRD7 restrains TNF-α-induced proliferation and migration of airway smooth muscle cells by inhibiting notch signaling.","authors":"Hong Li,&nbsp;Tian Yang,&nbsp;Tianjun Chen,&nbsp;Ya Liu,&nbsp;Yamei Pang,&nbsp;Lan Yang","doi":"10.1080/01902148.2022.2107730","DOIUrl":"https://doi.org/10.1080/01902148.2022.2107730","url":null,"abstract":"<p><p><b>Objective</b>: Bromodomain-containing protein 7 (BRD7) is a key component of the switch/sucrose non-fermentable complex that participates in chromatin remodeling and transcriptional regulation. Although the emerging role of BRD7 in the pathophysiology of various diseases has been observed, its role in asthma remains unknown. Here, we assessed the function of BRD7 as a mediator of airway remodeling in asthma using an <i>in vitro</i> model. <b>Methods:</b> Airway smooth muscle cells (ASMCs) were challenged with tumor necrosis factor-α (TNF-α) to establish an <i>in vitro</i> airway remodeling model. Protein levels were examined using western blotting. Cell proliferation was measured using the cell counting kit-8 and 5-ethynyl-2'-deoxyuridine assays. Cell migration was assessed using a transwell migration assay. <b>Results:</b> Exposure to TNF-α dramatically decreased BRD7 levels in ASMCs. BRD7 remarkably decreased TNF-α-induced proliferation and migration of ASMCs. In contrast, ASMCs with BRD7 deficiency were more sensitive to TNF-α-induced pro-proliferative and pro-migratory effects. Mechanistically, BRD7 could repress the expression of Notch1 and block the Notch pathway in TNF-α-challenged cells. Notably, reactivation of Notch signaling substantially reversed the BRD7 overexpression-mediated effects, whereas restraining Notch signaling abolished BRD7-depletion-mediated effects on TNF-α-challenged cells. <b>Conclusions:</b> BRD7 inhibits the proliferation and migration of ASMCs elicited by TNF-α by downregulating the Notch pathway. This study indicates that BRD7 may exert a suppressive effect on airway remodeling during asthma.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 7-8","pages":"199-212"},"PeriodicalIF":1.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40692631","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":"<i>Lef1</i> is transcriptionally activated by <i>Klf4</i> and suppresses hyperoxia-induced alveolar epithelial cell injury.","authors":"Min Yang,&nbsp;Xueshan Huang,&nbsp;Fang Shen,&nbsp;Juanjuan Yi,&nbsp;Yanni Meng,&nbsp;Yanping Chen","doi":"10.1080/01902148.2022.2108945","DOIUrl":"https://doi.org/10.1080/01902148.2022.2108945","url":null,"abstract":"<p><strong>Purpose: </strong>Bronchopulmonary dysplasia (BPD) is a long-term respiratory condition. More than a quarter of extremely premature newborns are harmed by BPD. At present, there are no apparent effective drugs or treatments for the condition. In this study, we aimed to investigate the functional role and mechanism of lymphoid enhancer-binding factor 1 (<i>Lef1</i>) in BPD <i>in vitro</i>.</p><p><strong>Materials and methods: </strong>Blood samples from BPD patients and healthy volunteers were gathered, and an <i>in vitro</i> model of BPD was developed in alveolar epithelial cells (AECs) MLE-12 induced by hyperoxia. Then expression of krüppel-like factor 4 (<i>KLF4</i>/<i>Klf4</i>) and <i>LEF1</i>/<i>Lef1</i> were evaluated. After <i>Lef1</i> overexpressing plasmid and the vector were transfected into hyperoxia-induced MLE-12 cells, cell proliferation assays were carried out. Cell apoptosis was investigated by a flow cytometry assay, and apoptosis related proteins Bcl-2, cleaved-caspase 3 and 9 were analyzed by a western blot assay. The binding between <i>Klf4</i> and <i>Lef1</i> promoter predicted on the JASPAR website was verified using luciferase and ChIP assays. For further study of the mechanism of <i>Klf4</i> and <i>Lef1</i> in BPD, gain-of-function experiments were performed.</p><p><strong>Results: </strong>The mRNA levels of <i>KLF4</i>/<i>Klf4</i> and <i>LEF1</i>/<i>Lef1</i> were diminished in clinical BPD serum samples and hyperoxia-induced MLE-12 cells. Overexpression of <i>Lef1</i> stimulated AEC proliferation and suppressed AEC apoptosis induced by hyperoxia. Mechanically, <i>Klf4</i> bound to <i>Lef1</i>'s promoter region and aids transcription. Moreover, the results of gain-of-function experiments supported that <i>Klf4</i> could impede AEC damage induced by hyperoxia via stimulating <i>Lef1</i>.</p><p><strong>Conclusion: </strong><i>Klf4</i> and <i>Lef1</i> expression levels were declined in hyperoxia-induced AECs, and <i>Lef1</i> could be transcriptionally activated by <i>Klf4</i> and protect against hyperoxia-induced AEC injury in BPD. As a result, <i>Lef1</i> might become a prospective therapeutic target for BPD.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 7-8","pages":"213-223"},"PeriodicalIF":1.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40685138","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":"Aerosol inhalation of <i>Mycobacterium vaccae</i> ameliorates airway structural remodeling in chronic asthma mouse model.","authors":"Qian-Nan Zhang,&nbsp;Huan Xiao,&nbsp;Li-Ting Fang,&nbsp;Qi-Xiang Sun,&nbsp;Lao-Dong Li,&nbsp;Si-Yue Xu,&nbsp;Chao-Qian Li","doi":"10.1080/01902148.2022.2115166","DOIUrl":"https://doi.org/10.1080/01902148.2022.2115166","url":null,"abstract":"<p><p><b>Background:</b> Airway remodeling is accepted to be a determining component within the natural history of asthma. Nebulized inhalation of <i>Mycobacterium vaccae</i> (<i>M. vaccae</i>) has a protective effect on asthmatic mice. However, little is known regarding the effect of <i>M. vaccae</i> on airway structural remodeling in asthmatic mice. The purpose of this study was to explore the effect and the underlying mechanism of <i>M. vaccae</i> aerosol inhalation on airway structural remodeling in an asthma mouse model. <b>Methods:</b> Chronic asthma mouse models were established by ovalbumin induction. The number of inflammatory cells in bronchoalveolar lavage fluid (BALF), pathological alterations in lung tissue, and levels of associated cytokines (IL-5, IL-13, TNF-α, and ovalbumin-specific immunoglobulin E [OVA-sIgE]) were all assessed after <i>M. vaccae</i> therapy. The relative expression of interleukin (IL)-1β, tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and Wnt1-induced signaling protein 1 (WISP1) mRNA were detected. Western blotting and immunohistochemistry detected the expression of Wnt/β-catenin pathway-related proteins in lung tissue. <b>Results:</b> <i>M. vaccae</i> aerosol inhalation relieved airway inflammation, airway hyper-responsiveness, and airway remodeling. <i>M. vaccae</i> reduced the levels of IL-5, IL-13, TNF-α, and OVA-sIgE in and downregulated the expression of IL-1β, TNF-α, NF-κB, and WISP1 mRNA in the pulmonary. In addition, <i>M. vaccae</i> inhibited the expression of β-catenin, WISP1, and Wnt1 protein and upregulated the expression of glycogen synthase kinase-3beta (GSK-3β). <b>Conclusion:</b> Nebulized inhalation of <i>M. vaccae</i> can reduce airway remodeling during asthma.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 7-8","pages":"239-250"},"PeriodicalIF":1.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412180","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":"Metabolic profile of exhaled breath condensate from the pneumonia patients","authors":"Xiaoguang Li, J. Du, Jing Chen, F. Lin, Wei Wang, Tingqiu Wei, Jie Xu, Q. Lu","doi":"10.1080/01902148.2022.2078019","DOIUrl":"https://doi.org/10.1080/01902148.2022.2078019","url":null,"abstract":"Abstract Purpose of the Study Exhaled breath condensate (EBC) is increasingly being used for disease diagnosis and environmental exposure assessment as a noninvasive method reducing the risk of exposure. The purpose of this study was to investigate the application of a new sample type of EBC in pneumonia by metabolomics and to explore differential metabolites and potential metabolic pathways. Materials and Methods A case-control study was performed at the Peking University Third Hospital from August to December 2020. C-MS/MS analyses were performed on EBC samples using a UHPLC system. Results Totally 22 patients with pneumonia and 24 healthy controls were recruited. Using untargeted metabolomics based on LC-MS/MS analysis, 25 kinds of differential metabolites were found. Through a comprehensive analysis of the pathways in which the differential metabolites were located, the key pathway with the highest correlation with the difference of metabolites was taurine and hypotaurine metabolism. Conclusions The study implicates that the hypotaurine/taurine metabolic pathway may play a role on the development of pneumonia through metabolism analysis on EBC and the 3-Sulfinoalanine may be used as a biomarker in the diagnosis of pneumonia.","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"149 - 157"},"PeriodicalIF":1.7,"publicationDate":"2022-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44151044","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":"TGF-β-induced CCR8 promoted macrophage transdifferentiation into myofibroblast-like cells.","authors":"Haijun Liu, Qingzhou Guan, Peng Zhao, Jiansheng Li","doi":"10.1080/01902148.2022.2055227","DOIUrl":"10.1080/01902148.2022.2055227","url":null,"abstract":"<p><p><b>Background:</b> Idiopathic pulmonary fibrosis (IPF) is an interstitial disease of unknown origin, characterized by tissue fibrosis, for which currently there is no effective treatment. Macrophages, the main immune cells in lung tissue, are involved in the whole process of pulmonary fibrosis. In recent years, intercellular transformation has led to wide spread concern among pulmonary fibrosis researchers. Macrophages with flexible heterogeneity and plasticity participate in different physiological processes in the body. Cell chemokine receptor 8 (CCR8) is expressed in a variety of cells and plays a significant chemotactic role in the induction of cell activation and migration. It can also promote the differentiation of macrophages under certain environmental conditions. The current study is intended to explore the role of CCR8 in macrophage to myofibroblast transdifferentiation (MMT) in IPF. <b>Methods:</b> We conducted experiments using CCR8-specific small interfering RNA (siRNA), an autophagy inhibitor (3-methyladenine, 3-MA), and an agonist (rapamycin) to explore the underlying mechanisms of macrophage transdifferentiation into myofibroblast cells in transforming growth factor-beta (TGF-β)-induced pulmonary fibrosis. <b>Results:</b> TGF-β treatment increased the CCR8 protein level in a time- and dose-dependent manner in mouse alveolar macrophages, as well as macrophage transdifferentiation-related markers, including vimentin, collagen 1, and a-SMA, and cell migration. In addition, the levels of autophagy were enhanced in macrophages treated with TGF-β. We found that 3-MA, an autophagy inhibitor, decreased the expression levels of macrophage transdifferentiation-related markers and attenuated cell migration. Furthermore, the inhibition of CCR8 via <i>CCR8</i>-specific siRNA reduced the levels of autophagy and macrophage transdifferentiation-related markers, and inhibited the cell migration. Enhancing autophagy with rapamycin attenuated the inhibition effect of <i>CCR8</i>-specific siRNA on macrophage migration and the increase in myofibroblast marker proteins. <b>Conclusions:</b> Our findings showed that the macrophages exposed to TGF-β had the potential to transdifferentiate into myofibroblasts and CCR8 was involved in the process. The effect of CCR8 on TGF-β-induced macrophage transdifferentiation occurs mainly through autophagy. Targeting CCR8 may be a novel therapeutic strategy for the treatment of IPF.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"1-14"},"PeriodicalIF":1.7,"publicationDate":"2022-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42416628","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":"SRC3 deficiency exacerbates lipopolysaccharide-induced acute respiratory distress syndrome in mice.","authors":"Meixia Cui, Shengtong Guo, Ying Cui","doi":"10.1080/01902148.2022.2104958","DOIUrl":"10.1080/01902148.2022.2104958","url":null,"abstract":"<p><p>Acute respiratory distress syndrome (ARDS) is a severe disease. Inflammation is the key element implicated in ARDS. Steroid receptor coactivator 3 (SRC3), a coactivator protein for transcription, is involved in regulation of inflammatory response. Here we explored the potential roles of SRC3 in ARDS. We utilized the SRC3 deficient (SRC3^-/-) mice and established the lipopolysaccharides (LPS)-induced ARDS model. The mortality, lung injury, leucocytes infiltration and inflammatory cytokine production were compared between wild type (WT) and SRC3^-/- mice. The NF-κB activation in lung of WT and SRC3^-/- mice was measured. After LPS treatment, SRC3^-/- mice had higher mortality and more severe lung damage than WT mice. LPS-treated SRC3^-/- mice had more leucocytes infiltration and upregulated inflammatory cytokine production. LPS-treated SRC3^-/- mice had elevated NF-κB activation. SRC3^-/- mice had exacerbated ARDS in LPS-treated mice.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":" ","pages":"178-186"},"PeriodicalIF":1.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40663696","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":"Pulmonary inflammation caused by cigarette smoke combined with lipopolysaccharide up-regulated OATP2B1 in rat lung tissue and pulmonary epithelial cells.","authors":"Zihao Wang, Xin Fang, Shuyi Zhang, Jue Song","doi":"10.1080/01902148.2022.2066223","DOIUrl":"10.1080/01902148.2022.2066223","url":null,"abstract":"<p><p>Organic anion transport polypeptide 2B1 (OATP2B1), as an uptake transporter, is involved in the transport of many related substrate drugs and endogenous substances in the lungs. A large amount of data shows that cigarette smoke plays an important role in the occurrence and development of lung diseases such as chronic obstructive pulmonary disease (COPD), asthma and bronchitis. However, the effect of cigarette smoke combined with lipopolysaccharide-induced pulmonary inflammation on the expression of OATP2B1 is not clear. In this study, we used cigarette smoke combined with lipopolysaccharide to establish a lung inflammation model in vivo and in vitro to explore the effect of inflammation on the expression of OATP2B1. Our study found that cigarette smoke combined with lipopolysaccharide-induced pulmonary inflammation upregulated the mRNA and protein expression of OATP2B1 and related inflammatory factors, and the expression level of related proteins was higher with the aggravation of inflammation. The experimental results of animals in vivo were consistent with those of cells in vitro. In summary, these findings provide a model and basis for a follow-up study of the mechanism of OATP2B1 in pulmonary inflammation.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"114-125"},"PeriodicalIF":1.7,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44766005","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}