scholarly journals Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners

2010 ◽  
Vol 298 (6) ◽  
pp. L857-L862 ◽  
Author(s):  
Laura Chimenti ◽  
Giuseppe Morici ◽  
Alessandra Paternò ◽  
Roberta Santagata ◽  
Anna Bonanno ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Induced Sputum ◽  
Intense Exercise ◽  
Bronchial Epithelial ◽  
Epithelial Damage ◽  
Peripheral Airways ◽  
Large Airways ◽  
Exercise In Humans

High neutrophil counts in induced sputum have been found in nonasthmatic amateur runners at rest and after a marathon, but the pathogenesis of airway neutrophilia in athletes is still poorly understood. Bronchial epithelial damage may occur during intense exercise, as suggested by investigations conducted in endurance-trained mice and competitive human athletes studied under resting conditions. To gain further information on airway changes acutely induced by exercise, airway cell composition, apoptosis, IL-8 concentration in induced sputum, and serum CC-16 level were measured in 15 male amateur runners at rest (baseline) and shortly after a half-marathon. Different from results obtained after a marathon, neutrophil absolute counts were unchanged, whereas bronchial epithelial cell absolute counts and their apoptosis increased significantly ( P < 0.01). IL-8 in induced sputum supernatants almost doubled postrace compared with baseline ( P < 0.01) and correlated positively with bronchial epithelial cell absolute counts ( R2 = 0.373, P < 0.01). Serum CC-16 significantly increased after all races ( P < 0.01). These data show mild bronchial epithelial cell injury acutely induced by intense endurance exercise in humans, extending to large airways the data obtained in peripheral airways of endurance-trained mice. Therefore, neutrophil influx into the airways of athletes may be secondary to bronchial epithelial damage associated with intense exercise.

scholarly journals MicroRNA-21 Mediates the Protective Effects of Mesenchymal Stem Cells Derived from iPSCs to Human Bronchial Epithelial Cell Injury Under Hypoxia

2018 ◽  
Vol 27 (3) ◽  
pp. 571-583 ◽  
Author(s):  
Cheng-Lin Li ◽  
Zhi-Bin Xu ◽  
Xing-Liang Fan ◽  
He-Xin Chen ◽  
Qiu-Ning Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Epithelial Cell ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Bronchial Epithelial ◽  
Epithelial Cell Injury

Airway epithelial cell injury is a key triggering event to activate allergic airway inflammation, such as asthma. We previously reported that administration of mesenchymal stem cells (MSCs) significantly alleviated allergic inflammation in a mouse model of asthma, and the mmu-miR-21/ACVR2A axis may be involved. However, whether MSCs protect against bronchial epithelial cell injury induced by hypoxia, and the underlying mechanism, remain unknown. In our study, the human bronchial epithelial cell line BEAS-2B was induced to undergo apoptosis with a hypoxia mimic of cobalt chloride (CoCl2) damage. Treatment of MSCs derived from induced pluripotent stem cells (iPSCs) significantly decreased apoptosis of BEAS-2B cells. There was high miR-21 expression in injured BEAS-2B cells after MSC treatment. Transfection of the miR-21 mimic significantly decreased apoptosis of BEAS-2B, and transfection of a miR-21 inhibitor significantly increased apoptosis. More importantly, the protective effects of MSCs on injured BEAS-2B were reversed by transfection of the miR-21 inhibitor. Binding sites of human miR-21 were identified in the 3’UTR of human ACVR2A. We further determined that CoCl2 stimulation increased ACVR2A expression at both the mRNA and protein levels. Moreover, transfection of the miR-21 mimic further up-regulated ACVR2A expression induced by CoCl2, whereas transfection of the miR-21 inhibitor down-regulated ACVR2A expression. In addition, MSCs increased ACVR2A expression in BEAS-2B cells; however, this effect was reversed after transfection of the miR-21 inhibitor. Our data suggested that MSCs protect bronchial epithelial cells from hypoxic injury via miR-21, which may represent an important target. These findings suggest the potentially wide application of MSCs for epithelial cell injury during hypoxia.

microRNA-218 Inhibits Lipopolysaccharide-Induced Bronchial Epithelial Cell Injury by Targeting E2F2

2020 ◽  
Vol 10 (8) ◽  
pp. 1161-1169
Author(s):  
Min Gong ◽  
Zhongmei Mao ◽  
Jinni Chen ◽  
Xin Ye ◽  
Xiaobing Zhou
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Stress Injury ◽  
Bronchial Epithelial ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

Acute bronchopneumonia is a common hospitalization disease in children and serious acute bronchopneumonia will lead to death of children. MicroRNAs (miRNAs) have been thought to be related to inflammation in many diseases. The present study aimed to investigate the relation between miR218 and E2F2 and the effect of miR-218 overexpression and E2F2 inhibition on the improvement of inflammation in LPS-induced bronchial epithelial cell. BEAS-2B cells were induced by LPS for 0, 6, 12, 24 and 48 h which the cell viability was analyzed by CCK-8 assay. The expression of miR-218 in LPS-induced bronchial epithelial cell and cell transfection was detected by RT-qPCR analysis. The levels of TNF-α, IL-1α, and IL-6 in BEAS2B cells were detected using commercially-available ELISA kits. The levels of ROS, MDA, SOD and LDH were detected by ROS assay kit and oxidative stress assay kit. The cell apoptosis was analyzed by flow cytometry analysis and DAPI and hochest staining. As a result, miR-218 was decreased in LPS-induced bronchial epithelial cell. With the time of LPS treatment extends, the cell viability was decreased. Overexpression of miR-218 reduced the expression of inflammatory cytokines and oxidative stress injury in LPS-induced BEAS2B cells. Overexpression of miR-218 reduced apoptosis of LPS-induced BEAS2B cells. E2F2 was demonstrated be a target of miR-218 which miR-218 overexpression could inhibit the expression of E2F2. E2F2 inhibition could reverse the inflammatory and oxidative stress injury of LPS-induced BEAS2B cells caused by miR-218 inhibition. E2F2 inhibition could reverse the apoptosis of LPS-induced BEAS2B cells caused by miR-218 inhibition. In addition, E2F2 inhibition could reverse the expression of p-STAT1, cleaved-caspase3 and cleaved-caspase9 in LPS-induced BEAS2B cells caused by miR-218 inhibition. In conclusion, this study indicated that miR-218 overexpression and E2F2 inhibition can alleviate the inflammation in LPS-induced bronchial epithelial cell, thereby decreasing the oxidative stress and cell apoptosis.

scholarly journals Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury

2019 ◽  
Vol 20 (7) ◽  
pp. 1678 ◽  
Author(s):  
Yi-Chen Lee ◽  
Chun-Yu Lin ◽  
Yen-Hsu Chen ◽  
Wen-Chin Chiu ◽  
Yen-Yun Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cell ◽  
Lung Injury ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Epithelial Cell Lines ◽  
Nfκb Pathway ◽  
Pro Inflammatory Cytokines

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.

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