Experimental Lung Research最新文献

{"title":"Preliminary bronchodilator dose effect on aerosol-delivery through different nebulizers in noninvasively ventilated COPD patients.","authors":"Yasmin M Madney, Hadeer S Harb, Thierry Porée, Myriam Eckes, Marina E Boules, Mohamed E A Abdelrahim","doi":"10.1080/01902148.2022.2047243","DOIUrl":"10.1080/01902148.2022.2047243","url":null,"abstract":"<p><p><b>Objectives:</b> This study aimed to evaluate the effect of a preliminary bronchodilator dose on the aerosol-d elivery by different nebulizers in noninvasively ventilated chronic obstructive pulmonary disease (COPD) patients. <b>Method:</b> COPD patients were randomized to receive study doses of 800 µg beclomethasone dipropionate (BPD) nebulized by either a vibrating mesh nebulizer (VMN) or a jet nebulizer (JN) connected to MinimHal spacer device. On a different day, the nebulized dose of beclomethasone was given to each patient by the same aerosol generator with and without preceded two puffs (100 µg each) of salbutamol delivered by a pressurized-metered dose inhaler. Urinary BPD and its metabolites in 30 min post-inhalation samples and pooled up to 24 h post-inhalation were measured. On day 2, ex-vivo studies were performed with BPD collected on filters before reaching patients which were eluted from filters and analyzed to estimate the total emitted dose.<b>Results:</b> The highest urinary excretion amounts of BPD and its metabolites 30 min and 24 h post-inhalation were identified with pMDI + VMN compared with other regimens(<i>p</i> < 0.001). The amounts of BPD and its metabolites excreted 30 min post inhalation had approximately doubled with pMDI + JN compared with JN delivery (<i>p</i> < 0.05). No significant effect was found in the ex-vivo study results except between VMN and JN with a significant superiority of the VMN (<i>p</i> < 0.001).<b>Conclusion:</b> Using a preliminary bronchodilator dose before drug nebulization significantly increased the effective lung dose of the nebulized drug with both VMNs and JNs. However, adding a preliminary bronchodilator dose increased the 24 hr cumulative urinary amount of the drug representing higher systemic delivery of the drug, which in turn could result in higher systemic side effects.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"1-9"},"PeriodicalIF":1.7,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42640473","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":"Bronchial epithelial SIRT1 deficiency exacerbates cigarette smoke induced emphysema in mice through the FOXO3/PINK1 pathway.","authors":"Hui Jiang, Yaona Jiang, Yuanri Xu, Dong Yuan, Yaqing Li","doi":"10.1080/01902148.2022.2037169","DOIUrl":"10.1080/01902148.2022.2037169","url":null,"abstract":"<p><p><b>Purpose:</b> Cellular senescence and mitochondrial fragmentation are thought to be crucial components of the cigarette smoke(CS)-induced responses that contribute to the chronic obstructive pulmonary disease (COPD) development as a result of accelerated premature aging of the lung. Although there have been a few reports on the role of sirtuin 1(SIRT1) in mitochondrial homeostasis, senescence and inflammation, whether SIRT1/FOXO3/PINK1 signaling mediated mitophagy ameliorates cellular senescence in COPD is still unclear. This study aimed to ascertain whether SIRT1 regulates cellular senescence via FOXO3/PINK1-mediated mitophagy in COPD. <b>Methods</b>: To investigate the effect of CS exposure and SIRT1 deficiency on mitophagy and senescence in the lung, a SIRT1 knockout(KO) mouse model was used. Airway resistance, cellular senescence mitochondrial injury, mitophagy, cellular architecture and protein expression levels in lung tissues, from SIRT1 KO and wild-type(WT) COPD model mice exposed to CS for 6 months were examined by western blotting, histochemistry, immunofluorescence and transmission electron microscopy(TEM). <b>Results</b>: In CS exposed mice, SIRT1 deficiency exacerbated airway resistance and cellular senescence, increased FOXO3 acetylation and decreased PINK1 protein levels and attenuated mitophagy. Mechanistically, the damaging effect of SIRT1 deficiency on lung tissue was attributed to increased FOXO3 acetylation and decreased PINK1 levels, and attenuated mitophagy. In vitro, mitochondrial damage and cellular sensitivity in response to CS exposure were more severe in control cells than in cells treated with aSIRT1 activator. SIRT1 activation SIRT1 activation decreased FOXO3 acetylation and increased the protein levels of PINK1 and enhanced mitophagy. <b>Conclusion</b>: These results demonstrated that the detrimental effects of SIRT1 deficiency on cell senescence associated with insufficient mitophagy, and involved the FOXO3/PINK1 signaling pathway.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":" ","pages":"1-16"},"PeriodicalIF":1.7,"publicationDate":"2022-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39602570","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":"The 16S rRNA lung microbiome in mechanically ventilated patients: a methodological study.","authors":"Melanie Fromentin,&nbsp;Antoine Bridier-Nahmias,&nbsp;Jérôme Legoff,&nbsp;Severine Mercier-Delarue,&nbsp;Noémie Ranger,&nbsp;Constance Vuillard,&nbsp;Julien Do Vale,&nbsp;Noémie Zucman,&nbsp;Antonio Alberdi,&nbsp;Jean-Damien Ricard,&nbsp;Damien Roux","doi":"10.1080/01902148.2021.2021327","DOIUrl":"https://doi.org/10.1080/01902148.2021.2021327","url":null,"abstract":"<p><strong>Purpose: </strong>Characterization of the respiratory tract bacterial microbiome is in its infancy when compared to the gut microbiota. To limit bias mandates a robust methodology. Specific amplification of the hypervariable (V) region of the 16SrRNA gene is a crucial step. Differences in accuracy exist for one V region to another depending on the sampled environment. We aimed to assess the impact of the primer sequences targeting the V4 region currently used for gut microbiota studies in respiratory samples. <b>Materials and methods</b>: The original 515 F-806R primer pair targets the V4 region of the 16SrRNA gene. We compared two different 515 F-806R primer pairs before Illumina 250 paired-end sequencing for bacterial microbiome analyses of respiratory samples from critically-ill ventilated patients. \"S-V4\" for \"Stringent V4\" primer pair is used in two ongoing international projects \"the Integrative Human microbiome project (iHMP)\" and \"the Earth microbiome project (EMP).\" \"R-V4\" for \"Relaxed V4\" primer pair has been modified to reduce biases against specific environmental taxa. The optimal method was determined by concordance with conventional microbiology. <b>Results</b>: Twenty samples from three patients who developed a ventilator-associated pneumonia (VAP) and four who did not (control ventilated patients) were sequenced. Highly different results were obtained. \"S-V4\" provided the best agreement with the conventional microbiology for endotracheal aspirate: 89% as compared to 56% for \"R-V4.\" The main difference related to poor <i>Enterobacteriaceae</i> detection with \"R-V4\" primers. <b>Conclusions:</b> Accuracy of the bacterial lung microbiome composition was highly dependent on the primers used for amplification of the 16 s rRNA hypervariable sequence. This work validates for future lung microbiome studies the use of the 515 F-806R \"S-V4\" primer pair associated to Illumina® MiSeq paired-end sequencing.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"23-34"},"PeriodicalIF":1.7,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39770067","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":"Effects of end-expiratory lung volume versus PaO₂ guided PEEP determination on respiratory mechanics and oxygenation in moderate to severe ARDS.","authors":"Kazim Rollas,&nbsp;Pervin Hanci,&nbsp;Arzu Topeli","doi":"10.1080/01902148.2021.2021326","DOIUrl":"https://doi.org/10.1080/01902148.2021.2021326","url":null,"abstract":"<p><p>There is no ideal method for determination of positive end-expiratory pressure (PEEP) in acute respiratory distress syndrome (ARDS) patients. We compared the effects of end-expiratory lung volume (EELV)-guided versus PaO₂-guided PEEP determination on respiratory mechanics and oxygenation during the first 48 hours in moderate to severe ARDS.</p><p><p>Twenty-two patients with moderate to severe ARDS admitted to an academic medical ICU were assigned to PaO₂-guided (<i>n</i> = 11) or to EELV-guided PEEP determination (<i>n</i> = 11) group. First, an incremental PEEP trial was performed by increasing PEEP by 3 cmH₂O steps from 8 to 20 cmH₂O and in each step EELV and lung mechanics were measured in both groups. Then, oxygenation and respiratory mechanics were measured under the determined PEEP at 4, 12, 24, and 48th hours.</p><p><p>After the incremental PEEP trial, over the 48 hours of the study period, in the EELV-guided group PaO₂ and PaO₂/FiO₂ increased (<i>p</i> = 0.04 and <i>p</i> = 0.02; respectively), whereas they did not change in PaO₂-guided group (<i>p</i> = 0.09 and <i>p</i> = 0.27; respectively). In all patients, the median value of EELV change (ΔEELV) during incremental PEEP trial was 25%. In patients with ΔEELV > 25% (<i>n</i> = 11) PaO₂, PaO₂/FiO₂ and Cs increased over time in 48 hours (<i>p</i> = 0.03, <i>p</i> < 0.01, and <i>p</i> = 0.04; respectively), whereas they did not change in those with ΔEELV ≤ 25% (<i>n</i> = 11) (<i>p</i> = 0.73, <i>p</i> = 0.51, and <i>p</i> = 0.73; respectively).</p><p><p>Compared to PaO₂-guided PEEP determination, EELV-guided PEEP determination resulted in greater improvement in oxygenation over time. Patients who had > 25% improvement in EELV during a PEEP trial had greater improvement in oxygenation and compliance over 48 hours.</p><p><p>Supplemental data for this article is available online at.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"12-22"},"PeriodicalIF":1.7,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39765715","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":"Overexpression of bone morphogenetic protein receptor type 2 suppresses transforming growth factor β-induced profibrotic responses in lung fibroblasts.","authors":"Jun Fukihara,&nbsp;Suzanne Maiolo,&nbsp;Jessica Kovac,&nbsp;Koji Sakamoto,&nbsp;Keiko Wakahara,&nbsp;Naozumi Hashimoto,&nbsp;Paul N Reynolds","doi":"10.1080/01902148.2021.2024301","DOIUrl":"https://doi.org/10.1080/01902148.2021.2024301","url":null,"abstract":"<p><strong>Materials and methods: </strong>We investigated BMPR2 expression in pulmonary fibrosis and TGF-β/BMP signaling in lung fibroblasts. Then we evaluated the impact of BMPR2 upregulation using adenoviral transduction on TGF-β-induced Smad2/3 phosphorylation and fibronectin production in lung fibroblasts.</p><p><strong>Results: </strong>BMPR2 was distributed in airway epithelium and alveolar walls in rat lungs. BMPR2 expression was decreased in fibrotic lesions in the lungs of rats with bleomycin-induced pulmonary fibrosis and in human lung fibroblasts (HLFs) stimulated with TGF-β. Although Smad2/3 phosphorylation and fibronectin production were not suppressed solely by BMPs, phosphorylated Smad2/3 was decreased in BMPR2-transduced cells even without BMP stimulation. Fibronectin was decreased only when BMPR2-transduced HLFs were stimulated with BMP7 (but not BMP4). Similar results were also observed in IPF patient HLFs and rat lung fibroblasts.</p><p><strong>Conclusions: </strong>BMPR2 expression was reduced in fibrotic lungs and lung fibroblasts stimulated with TGF-β. BMPR2 transduction to lung fibroblasts reduced Smad2/3 phosphorylation, and reduced fibronectin production when treated with BMP7. Upregulation of BMPR2 may be a possible strategy for treating pulmonary fibrosis.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"35-51"},"PeriodicalIF":1.7,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39916946","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":"Signal processing to remove spurious contributions to the assessment of respiratory mechanics.","authors":"Vitor Mori,&nbsp;Renato L Vitorasso,&nbsp;Vitor A Takeuchi,&nbsp;Wothan T Lima,&nbsp;Maria A Oliveira,&nbsp;Henrique T Moriya","doi":"10.1080/01902148.2021.2019355","DOIUrl":"https://doi.org/10.1080/01902148.2021.2019355","url":null,"abstract":"<p><p>Signal disruptions in small animals during the realization of the Forced Oscillation Technique are a well-known cause of data loss as it leads to non-reliable estimations of the respiratory impedance. In this work, we assessed the effects of removing the disrupted epoch when a 3-seconds input signal composed of one and a half 2-seconds full cycle is used.</p><p><p>We tested our hypothesis in 25 SAMR1 mice under different levels of bronchoconstriction due to methacholine administration by iv bolus injections in different doses (15 animals) and by iv continuous infusion in different infusion rates (10 animals). Signal disruptions were computationally simulated as sharp drops in the pressure signal within a short timescale, and signal processing was performed using own developed algorithms.</p><p><p>We found that the model goodness of fit worsens when averaging techniques to estimate the input respiratory impedance are not used. However, no statistically significant differences were observed in the comparison between Constant Phase Model parameters of the full 3-s signal and the 2-s non disrupted epoch in all doses or infusion rates for both methacholine delivery strategies.</p><p><p>The proposed technique presents reliable outcomes that can reduce animal use in Forced Oscillation Technique realization.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 1","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39747994","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":"Cell cycle kinase CHEK2 in macrophages alleviates the inflammatory response to <i>Staphylococcus aureus</i>-induced pneumonia.","authors":"Fei Xie,&nbsp;Ruidong Chen,&nbsp;Jie Zhao,&nbsp;Chunyan Xu,&nbsp;Chunxiang Zan,&nbsp;Bin Yue,&nbsp;Wenqiu Tian,&nbsp;Wenxia Yi","doi":"10.1080/01902148.2022.2029625","DOIUrl":"https://doi.org/10.1080/01902148.2022.2029625","url":null,"abstract":"<p><strong>Background: </strong>Excessive macrophage-mediated inflammation participates in the development of <i>Staphylococcus aureus</i> (<i>S. aureus</i>)-induced pneumonia. Checkpoint kinase 2 (Chek2) was screened out as macrophage-related infantile pneumonia gene after the differentially expressed analysis of RNAseq data derived from pam3CSK4 stimulated bone marrow-derived macrophages (BMDMs).</p><p><strong>Methods: </strong>RAW264.7 macrophage cells were transfected with Chek2-specific gRNA, which were further overexpressed with wide-type Chek2 or Chek2 kinase activity mutant (Chek2 KD, D368N). At the same time, the relative protein and mRNA expression of inflammatory cytokines were determined. C57BL/6J WT mice were intranasally infected with <i>S. aureus</i> to induce <i>S. aureus</i>-induced pneumonia, which was treated with BML-277, an inhibitor of Chek2. The symptoms of pneumonia mice and inflammatory cytokines associated with the nuclear factor kappa B (NF-κB) signaling pathways were further examined.</p><p><strong>Results: </strong><i>In vivo</i>, BML-277 significantly promoted pneumonia symptoms, including mortality, lung infiltration of immune cells, and the abundance of lung pro-inflammatory cytokines. Mechanically, BML-277 did not affect BMDMs survival but up-regulated the mRNA expression of tumor necrosis factor (Tnf), nitric oxide synthase 2 (Nos2), interleukin (Il)23a, and the secretion of Tnf-α and Il-23a. At the same time, genetic complementation experiment testified that Chek2 KD did not inhibit NF-κB and relevant inflammatory cytokines expression.</p><p><strong>Conclusion: </strong>Chek2 functions through the kinase mechanism to down-regulate the NF-κB pathway in macrophages to alleviate <i>S. aureus</i>-induced pneumonia in mice.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 2","pages":"53-60"},"PeriodicalIF":1.7,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9326771","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":"Cyclo-VEGI inhibits bronchial artery remodeling in a murine model of chronic asthma.","authors":"Kyung Hoon Kim,&nbsp;Jung Hur,&nbsp;Hwa Young Lee,&nbsp;Eung Gu Lee,&nbsp;Sook Young Lee","doi":"10.1080/01902148.2021.2015011","DOIUrl":"https://doi.org/10.1080/01902148.2021.2015011","url":null,"abstract":"<p><p><b>Purpose/Aim:</b> In the context of asthma, airway bronchial remodeling and angiogenesis in the bronchial mucosa are well established. Cyclopeptidic-vascular endothelial growth inhibitor (cyclo-VEGI) is an inhibitor of the vascular endothelial growth factor (VEGF) receptor that increases the proliferation of endothelial cells and the formation of new vessels. However, changes in the bronchial arteries of patients with asthma have not been clearly elucidated. We investigated whether structural changes occurred in bronchial arteries, as well as the effects of cyclo-VEGI in a mouse model of chronic asthma (<i>in vivo</i>) and human fibroblasts (<i>in vitro</i>). <b>Materials and Methods:</b> A validated mouse model of allergic airway inflammation with ovalbumin (OVA) as the causative allergen was used for the study. Mice were treated with cyclo-VEGI or fluticasone during OVA challenge. <i>In vitro</i> experiments were conducted to determine whether fibroblasts proliferated following elastin exposure and the effects of cyclo-VEGI on them. <b>Results:</b> OVA sensitization and challenge led to greater perivascular smooth muscle area, more elastic fibers, and elevated expression of vascular cell adhesion molecule (VCAM)-1 antigen. These phenomena indicated changes to bronchial arteries. Cyclo-VEGI and fluticasone treatment both inhibited airway hyper-responsiveness and inflammation. Cyclo-VEGI-treated mice exhibited decreased perivascular smooth muscle area, elastin fibers, and VCAM-1 expression. Fluticasone-treated mice exhibited reductions in perivascular smooth muscle but not in perivascular elastin or VCAM-1 expression. <i>In vitro</i>, fibroblast proliferation was enhanced by elastin treatment, which was inhibited by cyclo-VEGI treatment. Eotaxin expression was elevated in elastin-treated fibroblasts and decreased with cyclo-VEGI treatment. <b>Conclusions:</b> Vascular remodeling occurred in our mouse model of chronic asthma. Cyclo-VEGI could reduce airway inflammation and hyper-responsiveness by inhibiting VCAM-1 expression and elastin deposition around the bronchial arteries.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"47 10","pages":"494-506"},"PeriodicalIF":1.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39711659","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":"Nicotine associates to intracellular <i>Mycobacterium tuberculosis</i> inducing genes related with resistance to antimicrobial peptides.","authors":"Jeny de Haro-Acosta,&nbsp;Yolanda M Jacobo-Delgado,&nbsp;Adrian Rodríguez-Carlos,&nbsp;Flor Torres-Juárez,&nbsp;Zaida Araujo,&nbsp;Carmen J Serrano,&nbsp;Irma Gonzalez-Curiel,&nbsp;Rogelio Hernández-Pando,&nbsp;Eva Salinas,&nbsp;Bruno Rivas-Santiago","doi":"10.1080/01902148.2021.2006829","DOIUrl":"https://doi.org/10.1080/01902148.2021.2006829","url":null,"abstract":"<p><p>Tobacco consumption is related to an increased risk to develop tuberculosis. Antimicrobial peptides are essential molecules in the response to <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) because of their direct antimicrobial activity. The aim of this study was to demonstrate that nicotine enters into <i>Mtb</i> infected epithelial cells and associates with the mycobacteria inducing genes related to antimicrobial peptides resistance. Epithelial cells were infected with virulent <i>Mtb</i>, afterwards cells were stimulated with nicotine. The internalization of nicotine was followed using electron and confocal microscopy. The <i>lysX</i> expression was evaluated isolating mycobacterial RNA and submitted to RT-PCR analysis. Our results indicated that nicotine promotes <i>Mtb</i> growth in a dose-dependent manner in infected cells. We also reported that nicotine induces <i>lysX</i> expression. In conclusion, nicotine associates to intracellular mycobacteria promoting intracellular survival.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"47 10","pages":"487-493"},"PeriodicalIF":1.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39648737","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":"Continuous positive airway pressure affects mitochondrial function and exhaled PGC1-α levels in obstructive sleep apnea.","authors":"Ching-Chi Lin,&nbsp;Wei-Ji Chen,&nbsp;Yi-Kun Sun,&nbsp;Chung-Hsin Chiu,&nbsp;Mei-Wei Lin,&nbsp;I-Shiang Tzeng","doi":"10.1080/01902148.2021.2001607","DOIUrl":"https://doi.org/10.1080/01902148.2021.2001607","url":null,"abstract":"<p><p><b>Purpose:</b> Subjects with obstructive sleep apnea (OSA) exhibit systemic and upper airway oxidative stress and inflammation, which cause mitochondrial dysfunction. The intend of this study is to estimate mitochondrial function (mitochondrial DNA/nuclear DNA [Mt/N] ratio) and protein levels of peroxisome proliferator-coactivated receptor gamma co-activator 1-alpha (PGC1-α) in the exhaled breath condensate (EBC) and plasma before and after continuous positive airway pressure (CPAP) treatment. <b>Materials and methods:</b> Twenty healthy individuals (control) and 40 subjects with severe or moderate OSA were recruited to undergo CPAP treatment and evaluation in a sleep study. The Mt/N ratio in the EBC and blood were assayed by quantitative real-time polymerase chain reaction. Enzyme-linked immunosorbent assay was used to measure the protein concentration of PGC1-α in the EBC and plasma. All experiments were performed after 3 months of CPAP treatment in subjects with OSA. <b>Results:</b> We observed no noteworthy differences between the control and treatment groups. Moreover, there were no differences in the Mt/N ratio in the blood and plasma levels of PGC1-α in subjects with OSA before and after treatment. However, the Mt/N ratio and protein levels of PGC1-α in the EBC of OSA subjects were higher than those in the control group and returned to normal levels after CPAP treatment. <b>Conclusions:</b> We successfully treated subjects with OSA by CPAP, which restored the Mt/N ratio and levels of PGC1-α in the EBC.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"47 10","pages":"476-486"},"PeriodicalIF":1.7,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39611304","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}