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Alveolar epithelial injury

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https://www.readbyqxmd.com/read/29331644/ozone-exposure-induces-respiratory-barrier-biphasic-injury-and-inflammation-controlled-by-interleukin-33
#1
Chloé Michaudel, Claire Mackowiak, Isabelle Maillet, Louis Fauconnier, Cezmi Akdis, Milena Sokolowska, Anita Dreher, Hern-Tze Tina Tan, Valérie F Quesniaux, Bernhard Ryffel, Dieudonnée Togbe
BACKGROUND: IL-33 plays critical role in the regulation of tissue homeostasis, injury and repair. Whether IL-33 regulates neutrophil recruitment and function independently of airways hyperresponsiveness (AHR) in ozone induced lung injury and inflammation is unclear. OBJECTIVE: To examine the role of IL-33/ST2 axis in lung inflammation upon acute ozone exposure in mice. METHODS: ST2 and IL-33 deficient mice, IL-33-citrine reporter and C57BL/6 (WT) mice underwent a single ozone exposure (1 ppm for 1h) in all studies...
January 10, 2018: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29325098/high-level-of-neutrophil-extracellular-traps-correlates-with-poor-prognosis-of-severe-influenza-a-infection
#2
Liuluan Zhu, Lu Liu, Yue Zhang, Lin Pu, Jingyuan Liu, Xingwang Li, Zhihai Chen, Yu Hao, Beibei Wang, Junyan Han, Guoli Li, Shuntao Liang, Haofeng Xiong, Hong Zheng, Ang Li, Jianqing Xu, Hui Zeng
Background: Most patients with severe infection with influenza A virus (IAV) progress to acute respiratory distress syndrome and even multiple organ dysfunction syndrome (MODS). Neutrophil extracellular traps (NETs) can be induced by pathogens and are responsible for immune tissue damage. We conducted a prospective study on the production and effects of NETs in H7N9 and H1N1 patients. Methods: We investigated NET production in plasma and supernatant of cultured neutrophils by measuring cell-free deoxyribonucleic acid (DNA) and myeloperoxidase (MPO)-DNA complexes with PicoGreen dye and enzyme-linked immunosorbent assay methods, respectively...
January 9, 2018: Journal of Infectious Diseases
https://www.readbyqxmd.com/read/29324568/effects-of-pressure-support-ventilation-on-ventilator-induced-lung-injury-in-mild-acute-respiratory-distress-syndrome-depend-on-level-of-positive-end-expiratory-pressure
#3
Paulo A F Magalhães, Gisele de A Padilha, Lillian Moraes, Cíntia L Santos, Ligia de A Maia, Cassia L Braga, Maria do Carmo M B Duarte, Lívia B Andrade, Alberto Schanaider, Vera L Capellozzi, Robert Huhle, Marcelo Gama de Abreu, Paolo Pelosi, Patricia R M Rocco, Pedro L Silva
BACKGROUND: Harmful effects of spontaneous breathing have been shown in experimental severe acute respiratory distress syndrome (ARDS). However, in the clinical setting, spontaneous respiration has been indicated only in mild ARDS. To date, no study has compared the effects of spontaneous assisted breathing with those of fully controlled mechanical ventilation at different levels of positive end-expiratory pressure (PEEP) on lung injury in ARDS. OBJECTIVE: To compare the effects of assisted pressure support ventilation (PSV) with pressure-controlled ventilation (PCV) on lung function, histology and biological markers at two different PEEP levels in mild ARDS in rats...
January 10, 2018: European Journal of Anaesthesiology
https://www.readbyqxmd.com/read/29321022/serum-metabolic-profiling-identified-a-distinct-metabolic-signature-in-patients-with-idiopathic-pulmonary-fibrosis-a-potential-biomarker-role-for-lysopc
#4
Barbara Rindlisbacher, Cornelia Schmid, Thomas Geiser, Cédric Bovet, Manuela Funke-Chambour
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease of unknown etiology. Patients present loss of lung function, dyspnea and dry cough. Diagnosis requires compatible radiologic imaging and, in undetermined cases, invasive procedures such as bronchoscopy and surgical lung biopsy. The pathophysiological mechanisms of IPF are not completely understood. Lung injury with abnormal alveolar epithelial repair is thought to be a major cause for activation of profibrotic pathways in IPF...
January 10, 2018: Respiratory Research
https://www.readbyqxmd.com/read/29301259/sphingolipids-in-ventilator-induced-lung-injury-role-of-sphingosine-1-phosphate-lyase
#5
Vidyani Suryadevara, Panfeng Fu, David Lenin Ebenezer, Evgeny Berdyshev, Irina A Bronova, Long Shuang Huang, Anantha Harijith, Viswanathan Natarajan
Mechanical ventilation (MV) performed in respiratory failure patients to maintain lung function leads to ventilator-induced lung injury (VILI). This study investigates the role of sphingolipids and sphingolipid metabolizing enzymes in VILI using a rodent model of VILI and alveolar epithelial cells subjected to cyclic stretch (CS). MV (0 PEEP (Positive End Expiratory Pressure), 30 mL/kg, 4 h) in mice enhanced sphingosine-1-phosphate lyase (S1PL) expression, and ceramide levels, and decreased S1P levels in lung tissue, thereby leading to lung inflammation, injury and apoptosis...
January 1, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29290631/emodin-attenuates-bleomycin-induced-pulmonary-fibrosis-via-anti-inflammatory-and-anti-oxidative-activities-in-rats
#6
Sheng-Lan Tian, Yang Yang, Xiao-Liu Liu, Qing-Bang Xu
BACKGROUND Idiopathic pulmonary fibrosis (IPF) can severely damage lung function, which may result in death. Emodin is a major ingredient of rhubarb and has been proven to protect against lung disruptions. Our study focused on the potential medicinal effect of emodin against IPF. MATERIAL AND METHODS The experiment subjects were fully-grown male Sprague-Dawley rats with average weight of 180-220 kg. Histological analyses, Western blotting analysis, quantitative real-time PCR, and statistical analysis were used in the study...
January 1, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29277898/glucose-6-phosphate-dehydrogenase-inhibition-attenuates-acute-lung-injury-through-reduction-in-nadph-oxidase-derived-reactive-oxygen-species
#7
Ahmed Nadeem, Naif O Al-Harbi, Sheikh F Ahmad, Khalid E Ibrahim, Nahid Siddiqui, Mohammed M Al-Harbi
Acute lung injury (ALI) is a heterogeneous disease with the hallmarks of alveolar capillary membrane injury, increased pulmonary edema and pulmonary inflammation. The commonest direct etiological factor for ALI is usually parenchymal lung infection or hemorrhage. Reactive oxygen species (ROS) generated by NADPH oxidase (NOX2) are thought to play an important role in the pathophysiology of ALI. Glucose-6-phosphate dehydrogenase (G6PD) plays an important role both in production of ROS as well as their removal through supply of NADPH...
December 25, 2017: Clinical and Experimental Immunology
https://www.readbyqxmd.com/read/29273510/epigallocatechin-gallate-can-attenuate-human-alveolar-epithelial-cell-injury-induced-by-alpha-haemolysin
#8
Yonglin Zhou, Chengzhen Chen, Juan Pan, Xuming Deng, Jianfeng Wang
Staphylococcus aureus (S. aureus) is a common cause of hospital-acquired infection and has become an epidemic globally. Alpha-haemolysin (α-haemolysin), a pore-forming toxin, is one of the most important virulence factors secreted by most S. aureus strains. α-haemolysin monomers form a 232.4-kDa membrane-inserted heptamer by self-assembling to cause host cell lysis and death. Consequently, α-haemolysin plays a significant role in the pathogenesis of S. aureus, and it could be the target for the treatment of staphylococcal infection...
December 19, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/29246207/plasma-surfactant-protein-d-as-a-diagnostic-biomarker-for-acute-respiratory-distress-syndrome-validation-in-us-and-korean-cohorts
#9
Jinkyeong Park, Maria Pabon, Augustine M K Choi, Ilias I Siempos, Laura E Fredenburgh, Rebecca M Baron, Kyeongman Jeon, Chi Ryang Chung, Jeong Hoon Yang, Chi-Min Park, Gee Young Suh
BACKGROUND: Acute respiratory distress syndrome (ARDS) is potentially underrecognized by clinicians. Early recognition and subsequent optimal treatment of patients with ARDS may be facilitated by usage of biomarkers. Surfactant protein D (SP-D), a marker of alveolar epithelial injury, has been proposed as a potentially useful biomarker for diagnosis of ARDS in a few studies. We tried to validate the performance of plasma SP-D levels for diagnosis of ARDS. METHODS: We conducted a retrospective analysis using data from three (two in USA and one in Korea) prospective biobank cohorts involving 407 critically ill patients admitted to medical intensive care unit (ICU)...
December 15, 2017: BMC Pulmonary Medicine
https://www.readbyqxmd.com/read/29233858/enhancement-of-glycolysis-by-inhibition-of-oxygen-sensing-prolyl-hydroxylases-protects-alveolar-epithelial-cells-from-acute-lung-injury
#10
Kentaro Tojo, Nao Tamada, Yusuke Nagamine, Takuya Yazawa, Shuhei Ota, Takahisa Goto
Cellular bioenergetic failure caused by mitochondrial dysfunction is a key process of alveolar epithelial injury during acute respiratory distress syndrome (ARDS). Prolyl hydroxylases (PHDs) act as cellular oxygen sensors, and their inhibition activates hypoxia-inducible factor (HIF), resulting in enhanced cellular glycolytic activity, which could compensate for impaired mitochondrial function and protect alveolar epithelial cells from ARDS. Here, we evaluated the effects of pharmacological PHD inhibition with dimethyloxalylglycine (DMOG) on alveolar epithelial cell injury using in vitro and in vivo ARDS models...
December 12, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29229270/intratracheal-instillation-of-alveolar-type-ii-cells-enhances-recovery-from-acute-lung-injury-in-rats
#11
Raquel Guillamat-Prats, Ferranda Puig, Marta Camprubí-Rimblas, Raquel Herrero, Anna Serrano-Mollar, Maria Nieves Gómez, Jessica Tijero, Michael A Matthay, Lluís Blanch, Antonio Artigas
BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by excess production of inflammatory factors. Alveolar type II (ATII) cells help repair damaged lung tissue, rapidly proliferating and differentiating into alveolar type I cells after epithelial cell injury. In ALI, the lack of viable ATII favors progression to more severe lung injury. ATII cells regulate the immune response by synthesizing surfactant and other anti-inflammatory proteins and lipids...
November 8, 2017: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/29226550/alpha-klotho-enrichment-in-induced-pluripotent-stem-cell-secretome-contributes-to-antioxidative-protection-in-acute-lung-injury
#12
Amiq Gazdhar, Priya Ravikumar, Johanne Pastor, Manfred Heller, Jianfeng Ye, Jianning Zhang, Orson W Moe, Thomas Geiser, Connie C W Hsia
Induced pluripotent stem cells (iPSCs) has been reported to alleviate organ injury, although the mechanisms of action remain unclear and administration of intact cells faces many limitations. We hypothesized that cell-free conditioned media (CM) containing the secretome of iPSCs possess antioxidative constituents that can alleviate pulmonary oxidant stress damage. We derived iPSCs from human dermal fibroblasts and harvested the CM. Addition of iPSC CM to cultured human alveolar type-1 epithelial cells mitigated hyperoxia-induced depletion of endogenous total antioxidant capacity (TAC) while tracheal instillation of iPSC CM into adult rat lungs enhanced hyperoxia-induced increase in TAC...
December 11, 2017: Stem Cells
https://www.readbyqxmd.com/read/29222007/current-concepts-in-pathogenesis-diagnosis-and-management-of-smoking-related-interstitial-lung-diseases
#13
REVIEW
Anupam Kumar, Sujith V Cherian, Robert Vassallo, Eunhee S Yi, Jay H Ryu
Tobacco exposure results in various changes to the airways and lung parenchyma. While emphysema represents the more common injury pattern, in some individuals, cigarette smoke injures alveolar epithelial and other lung cells resulting in diffuse infiltrates and parenchymal fibrosis. Smoking can trigger interstitial injury patterns mediated via recruitment and inappropriate persistence of myeloid and other immune cells including eosinophils. As our understanding of the role of cigarette smoke constituents in triggering lung injury continues to evolve, so does our recognition of the spectrum of smoking-related interstitial lung changes...
December 5, 2017: Chest
https://www.readbyqxmd.com/read/29218325/protection-of-meconium-induced-lung-epithelial-injury-by-protease-inhibitors
#14
C Ota, I Gopallawa, V Ivanov, I H Gewolb, B D Uhal
Earlier work form this laboratory showed that exposure of alveolar epithelial cells (AECs) to meconium caused significant cell detachment and that meconium-induced detachment of cells was prevented by a protease inhibitor cocktail. Therefore, it was hypothesized that protease inhibitors might protect AEC monolayers against meconium-induced collapse of epithelial barrier function both in vitro and in vivo. To investigate this theory in vitro, albumin flux was measured across cultured, confluent monolayers of human type II derived cell line A549 on microporous filter inserts...
2017: Journal of Lung, Pulmonary & Respiratory Research
https://www.readbyqxmd.com/read/29210175/site-specific-and-endothelial-mediated-dysfunction-of-the-alveolar-capillary-barrier-in-response-to-lipopolysaccharides
#15
Harshavardhan Janga, Liam Cassidy, Fanlu Wang, Dietmar Spengler, Stefanie Oestern-Fitschen, Martin F Krause, Andreas Seekamp, Andreas Tholey, Sabine Fuchs
Infectious agents such as lipopolysaccharides (LPS) challenge the functional properties of the alveolar-capillary barrier (ACB) in the lung. In this study, we analyse the site-specific effects of LPS on the ACB and reveal the effects on the individual cell types and the ACB as a functional unit. Monocultures of H441 epithelial cells and co-cultures of H441 with endothelial cells cultured on Transwells® were treated with LPS from the apical or basolateral compartment. Barrier properties were analysed by the transepithelial electrical resistance (TEER), by transport assays, and immunostaining and assessment of tight junctional molecules at protein level...
December 5, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29206808/extrinsic-calcitonin-gene-related-peptide-inhibits-hyperoxia-induced-alveolar-epithelial-type-ii-cells-apoptosis-oxidative-stress-and-reactive-oxygen-species-ros-production-by-enhancing-notch-1-and-homocysteine-induced-endoplasmic-reticulum-protein-herp-expression
#16
Yu-Xin Bai, Fang Fang, Jia-Ling Jiang, Feng Xu
BACKGROUND Lung alveolar epithelial type II cells (AEC II) are the most important stem cells in lung tissues, which are critical for wound repair of bronchopulmonary dysplasia (BPD). This study investigated the effects of calcitonin gene-related peptide (CGRP) on AEC II cells exposed to hyperoxia. MATERIAL AND METHODS Neonatal rat AEC II cells were isolated and identified by detecting surfactant protein C (SP-C). Three small interfering RNAs targeting Notch 1 were synthesized and transfected into AEC II. A hyperoxia-exposed AEC II cell injury model was established and was divided into 8 groups...
December 5, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29200204/thyroid-hormone-inhibits-lung-fibrosis-in-mice-by-improving-epithelial-mitochondrial-function
#17
Guoying Yu, Argyris Tzouvelekis, Rong Wang, Jose D Herazo-Maya, Gabriel H Ibarra, Anup Srivastava, Joao Pedro Werneck de Castro, Giuseppe DeIuliis, Farida Ahangari, Tony Woolard, Nachelle Aurelien, Rafael Arrojo E Drigo, Ye Gan, Morven Graham, Xinran Liu, Robert J Homer, Thomas S Scanlan, Praveen Mannam, Patty J Lee, Erica L Herzog, Antonio C Bianco, Naftali Kaminski
Thyroid hormone (TH) is critical for the maintenance of cellular homeostasis during stress responses, but its role in lung fibrosis is unknown. Here we found that the activity and expression of iodothyronine deiodinase 2 (DIO2), an enzyme that activates TH, were higher in lungs from patients with idiopathic pulmonary fibrosis than in control individuals and were correlated with disease severity. We also found that Dio2-knockout mice exhibited enhanced bleomycin-induced lung fibrosis. Aerosolized TH delivery increased survival and resolved fibrosis in two models of pulmonary fibrosis in mice (intratracheal bleomycin and inducible TGF-β1)...
December 4, 2017: Nature Medicine
https://www.readbyqxmd.com/read/29198702/hydrogen-protects-against-hyperoxia-induced-apoptosis-in-type-ii-alveolar-epithelial-cells-via-activation-of-pi3k-akt-foxo3a-signaling-pathway
#18
Dan Wu, Mulin Liang, Hongxing Dang, Fang Fang Feng Xu, Chengjun Liu
Oxidative stress is regarded as a key regulator in the pathogenesis of prolonged hyperoxia-induced lung injury, which causes injury to alveolar epithelial cells and eventually leads to development of bronchopulmonary dysplasia (BPD). Many studies have shown that hydrogen has a protective effect in a variety of cells. However, the mechanisms by which hydrogen rescues cells from damage due to oxidative stress in BPD remains to be fully elucidated. This study sought to evaluate the effects of hydrogen on hyperoxia-induced lung injury and to investigate the underlying mechanism...
November 30, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29191391/biphasic-lung-injury-during-streptococcus-pneumoniae-infection-in-a-murine-model
#19
A Prevotat, C Rouyer, P Gosset, E Kipnis, K Faure, B Guery
OBJECTIVES: Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. We aimed to analyze the epithelial response to S. pneumoniae-induced lung injury. METHODS: Using an in vitro model with 16HBE cells and experimental in vivo murine model of acute lung injury, we analyzed the epithelial response to S. pneumoniae. Lung epithelial cell monolayers were exposed to S. pneumoniae and permeability was assessed by transepithelial resistance (TER) measurement and organization and expression of junction proteins...
November 27, 2017: Médecine et Maladies Infectieuses
https://www.readbyqxmd.com/read/29180999/alarmin-s100a8-activates-alveolar-epithelial-cells-in-the-context-of-acute-lung-injury-in-a-tlr4-dependent-manner
#20
Deblina Chakraborty, Stefanie Zenker, Jan Rossaint, Anna Hölscher, Michele Pohlen, Alexander Zarbock, Johannes Roth, Thomas Vogl
Alveolar epithelial cells (AECs) are an essential part of the respiratory barrier in lungs for gas exchange and protection against pathogens. Damage to AECs occurs during lung injury and PAMPs/DAMPs have been shown to activate AECs. However, their interplay as well as the mechanism of AECs' activation especially by the alarmin S100A8/A9 is unknown. Thus, our aim was to study the mechanism of activation of AECs (type I and type II) by S100A8 and/or lipopolysaccharide (LPS) and to understand the role of endogenous S100A8/A9 in neutrophil recruitment in the lung...
2017: Frontiers in Immunology
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