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Alveolar epithelial injury

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https://www.readbyqxmd.com/read/28526890/a-heteromeric-molecular-complex-regulates-the-migration-of-lung-alveolar-epithelial-cells-during-wound-healing
#1
Manik C Ghosh, Patrudu S Makena, Joseph Kennedy, Bin Teng, Charlean Luellen, Scott E Sinclair, Christopher M Waters
Alveolar type II epithelial cells (ATII) are instrumental in early wound healing in response to lung injury, restoring epithelial integrity through spreading and migration. We previously reported in separate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor CXCR4 promote epithelial repair mechanisms. However, potential interactions between these two pathways were not previously considered. In the present study, we found that wounding of rat ATII cells promoted increased association between FAK and CXCR4...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28522567/myeloid-epithelial-crosstalk-coordinates-synthesis-of-the-tissue-protective-cytokine-leukemia-inhibitory-factor-during-pneumonia
#2
Katrina E Traber, Elise M Symer, Eri Allen, Yuri Kim, Kristie L Hilliard, Gregory A Wasserman, Colin L Stewart, Matthew R Jones, Joseph P Mizgerd, Lee Joseph Quinton
In bacterial pneumonia, lung damage resulting from epithelial cell injury is a major contributor to the severity of disease, and in some cases, can lead to long-term sequelae, especially in the setting of severe lung injury or ARDS. Leukemia inhibitory factor (LIF), a member of the IL-6 cytokine family, is a critical determinant of lung tissue protection during pneumonia, but the cellular sources of LIF and the signaling pathways leading to its production in the infected lung are not known. Here, we demonstrate that lung epithelium, specifically alveolar type II cells, is the predominant site of LIF transcript induction in pneumonic mouse lungs...
May 18, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28512431/variable-ventilation-improved-respiratory-system-mechanics-and-ameliorated-pulmonary-damage-in-a-rat-model-of-lung-ischemia-reperfusion
#3
André Soluri-Martins, Lillian Moraes, Raquel S Santos, Cintia L Santos, Robert Huhle, Vera L Capelozzi, Paolo Pelosi, Pedro L Silva, Marcelo Gama de Abreu, Patricia R M Rocco
Lung ischemia-reperfusion injury remains a major complication after lung transplantation. Variable ventilation (VV) has been shown to improve respiratory function and reduce pulmonary histological damage compared to protective volume-controlled ventilation (VCV) in different models of lung injury induced by endotoxin, surfactant depletion by saline lavage, and hydrochloric acid. However, no study has compared the biological impact of VV vs. VCV in lung ischemia-reperfusion injury, which has a complex pathophysiology different from that of other experimental models...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28511573/inhibition-of-pkr-ameliorates-lipopolysaccharide-induced-acute-lung-injury-by-suppressing-nf-%C3%AE%C2%BAb-pathway-in-mice
#4
Yinjiao Li, Jinglei Xiao, Yongchang Tan, Jun Wang, Yan Zhang, Xiaoming Deng, Yan Luo
Acute lung injury (ALI) is characterized by dramatic lung inflammation and alveolar epithelial cell death. Although protein kinase R (PKR) (double-stranded RNA-activated serine/threonine kinase) has been implicated in inflammatory response to bacterial cell wall components, whether it plays roles in lipopolysaccharide (LPS)-induced ALI remains unclear. This study was aimed to reveal whether and how PKR was involved in LPS-induced ALI pathology and the potential effects of its specific inhibitor, C16 (C13H8N4OS)...
May 17, 2017: Immunopharmacology and Immunotoxicology
https://www.readbyqxmd.com/read/28509332/myeloid-but-not-epithelial-tissue-factor-exerts-protective-anti-inflammatory-properties-in-acid-aspiration-induced-acute-lung-injury
#5
J B Kral-Pointner, W C Schrottmaier, V Horvath, H Datler, L Hell, C Ay, B Niederreiter, B Jilma, J A Schmid, A Assinger, N Mackman, S Knapp, G Schabbauer
INTRODUCTION: Acute lung injury (ALI) is a life-threatening condition characterized by damaged alveolar-capillary structures and activation of inflammatory and hemostatic processes. Tissue factor (TF) represents a crucial link between inflammation and coagulation, as inflammatory mediators induce myeloid TF expression and TF initiates the extrinsic coagulation. OBJECTIVE: Since pulmonary inflammation stimulates TF expression and TF modulates immune responses, we aimed to elucidate its impact on ALI...
May 16, 2017: Journal of Thrombosis and Haemostasis: JTH
https://www.readbyqxmd.com/read/28500076/stat5-is-required-for-cd103-dendritic-cell-and-alveolar-macrophage-development-and-protection-from-lung-injury
#6
William E Eddy, Ke-Qin Gong, Bryan Bell, William C Parks, Steven F Ziegler, Anne M Manicone
We tested the role of Stat5 in dendritic cell and alveolar macrophage (AM) homeostasis in the lung using CD11c-cre mediated deletion (Cre(+)5(f/f)). We show that Stat5 is required for CD103(+) dendritic cell and AM development. We found that fetal monocyte maturation into AMs was impaired in Cre(+)5(f/f) mice, and we also confirmed impaired AM development of progenitor cells using mixed chimera experiments. In the absence of Stat5 signaling in AMs, mice developed alveolar proteinosis with altered lipid homeostasis...
May 12, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28493081/regulation-of-inos-derived-ros-generation-by-hsp90-and-cav-1-in-porcine-reproductive-and-respiratory-syndrome-virus-infected-swine-lung-injury
#7
Meiping Yan, Make Hou, Jie Liu, Songlin Zhang, Bang Liu, Xiaoxiong Wu, Guoquan Liu
In the lungs, endothelial nitric oxide synthase (eNOS) is usually expressed in endothelial cells and inducible nitric oxide synthase (iNOS) is mainly expressed in alveolar macrophages and epithelial cells. Both eNOS and iNOS are involved in lung inflammation. While they play several roles in lung inflammation formation and resolution, their expression and activity are also regulated by inflammatory factors. Their expression relationship in virus infection-induced lung injury is not well addressed. In this report, we analyzed expression of both eNOS and iNOS, the production of nitric oxide (NO) and reactive oxygen species (ROS), and expression of their associated regulatory proteins, heat shock protein 90 (HSP90) and caveolin-1 (Cav-1), in a swine lung injury model induced by porcine reproductive and respiratory syndrome virus (PRRSV) infection...
May 10, 2017: Inflammation
https://www.readbyqxmd.com/read/28467984/neutrophil-extracellular-traps-stimulate-proinflammatory-responses-in-human-airway-epithelial-cells
#8
Florencia Sabbione, Irene A Keitelman, Leonardo Iula, Mariana Ferrero, Mirta N Giordano, Pablo Baldi, Martín Rumbo, Carolina Jancic, Analía S Trevani
Tissue injury leads to the release of uric acid (UA). At high local concentrations, UA can form monosodium urate crystals (MSU). MSU and UA stimulate neutrophils to release extracellular traps (NET). Here, we investigated whether these NET could be involved in the development of inflammation by stimulating cytokine release by airway epithelial cells. We found that NET significantly increased the secretion of CXCL8/IL-8 and IL-6 by alveolar and bronchial epithelial cells. These effects were not observed when NETosis was inhibited by Diphenyleneiodonium, elastase inhibitor, or Cl-amidine...
May 4, 2017: Journal of Innate Immunity
https://www.readbyqxmd.com/read/28459398/-effect-of-mechanical-stretch-preconditioning-on-pathological-stretch-induced-activation-of-%C3%AE-aminobutyric-acid-signaling-pathway-in-human-type-ii-alveolar-epithelial-cells
#9
Ke Luo, Luojing Zhou, Tianfeng Huang, Weizhen Guo, Ju Gao
OBJECTIVE: To evaluate the effect of mechanical stretch preconditioning on pathological stretch-induced activation of γ-aminobutyric acid (GABA) signaling pathway in human type II alveolar epithelial cells (AEC II). METHODS: AEC II cell line (A549 cells) cultured in vitro were divided into control group (group C), pathological stretch group (group P1) and mechanical stretch preconditioning group (group P2). In group C, A549 cells were cultured routinely. In group P1, A549 cells were exposed to 20% cyclic stretch for 6 hours...
January 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28459395/-role-and-mechanism-of-mitophagy-in-ventilator-induced-lung-injury-in-rats
#10
Ren Jing, Linghui Pan
OBJECTIVE: To explore the role and mechanism of mitophagy in ventilator-induced lung injury (VILI) in rats. METHODS: Thirty-six adult Sprague-Dawley (SD) rats were randomly divided into three groups (each n = 12): spontaneous breathing group (CON group), normal tidal volume (VT) group (NVT group, VT was 8 mL/kg) and high VT group (HVT group, VT was 40 mL/kg). All rats received endotracheal tube by tracheostomy. The rats in CON group were maintained spontaneous breathing, while those in NVT and HVT groups received mechanical ventilation with corresponding VT...
January 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28458673/inflammatory-responses-regulating-alveolar-ion-transport-during-pulmonary-infections
#11
REVIEW
Christin Peteranderl, Jacob I Sznajder, Susanne Herold, Emilia Lecuona
The respiratory epithelium is lined by a tightly balanced fluid layer that allows normal O2 and CO2 exchange and maintains surface tension and host defense. To maintain alveolar fluid homeostasis, both the integrity of the alveolar-capillary barrier and the expression of epithelial ion channels and pumps are necessary to establish a vectorial ion gradient. However, during pulmonary infection, auto- and/or paracrine-acting mediators induce pathophysiological changes of the alveolar-capillary barrier, altered expression of epithelial Na,K-ATPase and of epithelial ion channels including epithelial sodium channel and cystic fibrosis membrane conductance regulator, leading to the accumulation of edema and impaired alveolar fluid clearance...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28451868/juglone-alleviates-pneumolysin-induced-human-alveolar-epithelial-cell-injury-via-inhibiting-the-hemolytic-activity-of-pneumolysin
#12
Meng Song, Gejin Lu, Meng Li, Xuming Deng, Jianfeng Wang
Streptococcus pneumoniae (the pneumococcus) is an opportunistic pathogen responsible for several human diseases, including acute otitis media, pneumonia, sepsis and bacterial meningitis, and possesses numerous virulence factors associated with pneumococcal infection and pathogenesis. With the capacity to form pores in cholesterol-rich membranes, pneumolysin (PLY) is a key virulence factor of S. pneumoniae and causes severe tissue damage during pneumococcal infection. Juglone (JG), a natural 1,4-naphthoquinone widely found in the roots, leaves, woods and fruits of Juglandaceae walnut trees, inhibits PLY-induced hemolysis via inhibition of the oligomerization of PLY and exhibits minimal anti-S...
April 27, 2017: Antonie Van Leeuwenhoek
https://www.readbyqxmd.com/read/28451794/comparison-of-long-term-prognosis-and-relapse-of-dermatomyositis-complicated-with-interstitial-pneumonia-according-to-autoantibodies-anti-aminoacyl-trna-synthetase-antibodies-versus-anti-melanoma-differentiation-associated-gene-5-antibody
#13
Kentaro Isoda, Takuya Kotani, Tohru Takeuchi, Takao Kiboshi, Kenichiro Hata, Takaaki Ishida, Kenichiro Otani, Takao Kamimori, Hiroshi Fujiwara, Takeshi Shoda, Shigeki Makino
The aim of this study was to investigate long-term prognosis and relapse of dermatomyositis complicated with interstitial pneumonia (DMIP) according to anti-aminoacyl tRNA synthetase (ARS) antibodies and anti-melanoma differentiation-associated gene 5 (MDA5) antibody. This retrospective study comprised 36 patients with DMIP who were divided into the anti-ARS antibody-positive group (ARS+) (n = 12), anti MDA5 antibody-positive group (MDA5+) (n = 11), double-negative group (ARS-/MDA5-) (n = 11), and double-positive group (ARS+/MDA5+) (n = 1)...
April 27, 2017: Rheumatology International
https://www.readbyqxmd.com/read/28442445/cyclic-mechanical-stretch-induced-oxidative-stress-occurs-via-a-nox-dependent-mechanism-in-type-ii-alveolar-epithelial-cells
#14
Toru Tanaka, Yoshinobu Saito, Kuniko Matsuda, Koichiro Kamio, Shinji Abe, Kaoru Kubota, Arata Azuma, Akihiko Gemma
Cyclic mechanical stretching (CMS) of the alveolar epithelium is thought to contribute to alveolar epithelial injury through an increase in oxidative stress. The aim of this study was to investigate the mechanisms of CMS-induced oxidative stress in alveolar epithelial cells (AECs). A549 cells were subjected to CMS, and the levels of 8-isoprostane and 3-nytrotyrosine were measured. Twenty-four hours of CMS induced a significant increase in the levels of 8-isoprostane and 3-nytrotyrosine. Although CMS did not increase the xanthine oxidase activity or the mitochondrial production of reactive oxygen species, it upregulated the expression of nicotine adenine dinucleotide phosphate oxidase (NOX) 2, 4, 5 and DUOX2...
April 22, 2017: Respiratory Physiology & Neurobiology
https://www.readbyqxmd.com/read/28439270/cytokine-regulation-of-na-k-cl-cotransporter-1-and-cystic-fibrosis-transmembrane-conductance-regulator-potential-role-in-pulmonary-inflammation-and-edema-formation
#15
REVIEW
Sarah Weidenfeld, Wolfgang M Kuebler
Pulmonary edema, a major complication of lung injury and inflammation, is defined as accumulation of extravascular fluid in the lungs leading to impaired diffusion of respiratory gases. Lung fluid balance across the alveolar epithelial barrier protects the distal airspace from excess fluid accumulation and is mainly regulated by active sodium transport and Cl(-) absorption. Increased hydrostatic pressure as seen in cardiogenic edema or increased vascular permeability as present in inflammatory lung diseases such as the acute respiratory distress syndrome (ARDS) causes a reversal of transepithelial fluid transport resulting in the formation of pulmonary edema...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28438162/targeting-of-nicotinamide-phosphoribosyltransferase-enzymatic-activity-ameliorates-lung-damage-induced-by-ischemia-reperfusion-in-rats
#16
Geng-Chin Wu, Wen-I Liao, Shu-Yu Wu, Hsin-Ping Pao, Shih-En Tang, Min-Hui Li, Kun-Lun Huang, Shi-Jye Chu
BACKGROUND: Emerging evidence reveals that nicotinamide phosphoribosyltransferase (NAMPT) has a significant role in the pathophysiology of the inflammatory process. NAMPT inhibition has a beneficial effect in the treatment of a variety of inflammatory diseases. However, it remains unclear whether NAMPT inhibition has an impact on ischemia-reperfusion (I/R)-induced acute lung injury. In this study, we examined whether NAMPT inhibition provided protection against I/R lung injury in rats...
April 24, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28428003/rac1-signaling-regulates-cigarette-smoke-induced-inflammation-in-the-lung-via-the-erk1-2-mapk-and-stat3-pathways
#17
Jun-Xia Jiang, Shui-Juan Zhang, Hui-Juan Shen, Yan Guan, Qi Liu, Wei Zhao, Yong-Liang Jia, Jian Shen, Xiao-Feng Yan, Qiang-Min Xie
Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Our previous studies have indicated that Rac1 is involved in lipopolysaccharide-induced pulmonary injury and CS-mediated epithelial-mesenchymal transition. However, the contribution of Rac1 activity to CS-induced lung inflammation remains not fully clear. In this study, we investigated the regulation of Rac1 in CS-induced pulmonary inflammation. Mice or 16HBE cells were exposed to CS or cigarette smoke extract (CSE) to induce acute inflammation...
April 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28427999/serpinb1-ameliorates-acute-lung-injury-in-liver-transplantation-through-erk1-2-mediated-stat3-dependent-ho-1-induction
#18
Weifeng Yao, Haobo Li, Gangjian Luo, Xiang Li, Chaojin Chen, Dongdong Yuan, Xinjin Chi, Zhengyuan Xia, Ziqing Hei
BACKGROUND: Postoperative acute lung injury (ALI) is a severe complication after liver transplantation, which severely affects postoperative patients' survival. The underlying mechanism is largely unknown and effective treatment limited. We explored the role of serpin protease inhibitor B1 (SERPINB1), a potent inhibitor of neutrophil serine proteases, in ALI in liver transplantation and its interplay with signal transducer and activator of transcription 3 (STAT3) and heme oxygenase-1 (HO-1)...
April 17, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28426693/influence-of-prenatal-hypoxia-and-postnatal-hyperoxia-on-morphologic-lung-maturation-in-mice
#19
Andreas Schmiedl, Torge Roolfs, Erol Tutdibi, Ludwig Gortner, Dominik Monz
BACKGROUND: Oxygen supply as a lifesaving intervention is frequently used to treat preterm infants suffering additionally from possible prenatal or perinatal pathogen features. The impact of oxygen and/or physical lung injury may influence the morphological lung development, leading to a chronic postnatal lung disease called bronchopulmonary dysplasia (BPD). At present different experimental BPD models are used. However, there are no systematic comparative studies regarding different influences of oxygen on morphological lung maturation...
2017: PloS One
https://www.readbyqxmd.com/read/28426531/high-fat-feeding-protects-mice-from-ventilator-induced-lung-injury-via-neutrophil-independent-mechanisms
#20
Michael R Wilson, Joanne E Petrie, Michael W Shaw, Cong Hu, Charlotte M Oakley, Samantha J Woods, Brijesh V Patel, Kieran P O'Dea, Masao Takata
OBJECTIVE: Obesity has a complex impact on acute respiratory distress syndrome patients, being associated with increased likelihood of developing the syndrome but reduced likelihood of dying. We propose that such observations are potentially explained by a model in which obesity influences the iatrogenic injury that occurs subsequent to intensive care admission. This study therefore investigated whether fat feeding protected mice from ventilator-induced lung injury. DESIGN: In vivo study...
April 19, 2017: Critical Care Medicine
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