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通气样机械应变调节 BEAS2B 上皮细胞的炎症反应。

Ventilation-Like Mechanical Strain Modulates the Inflammatory Response of BEAS2B Epithelial Cells.

机构信息

Department of Anesthesiology and Critical Care, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Germany.

出版信息

Oxid Med Cell Longev. 2019 Jun 19;2019:2769761. doi: 10.1155/2019/2769761. eCollection 2019.

DOI:10.1155/2019/2769761
PMID:31320981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6607724/
Abstract

Protective mechanical ventilation is aimed at preventing ventilator-induced lung injury while ensuring sufficient gas exchange. A new approach focuses on the temporal profile of the mechanical ventilation. We hypothesized that the temporal mechanical strain profile modulates inflammatory signalling. We applied cyclic strain with various temporal profiles to human bronchial epithelial cells (BEAS2B) and assessed proinflammatory response. The cells were subjected to sinusoidal, rectangular, or triangular strain profile and rectangular strain profile with prestrain set to 0, 25, 50, or 75% of the maximum stain, static strain, and strain resembling a mechanical ventilation-like profile with or without flow-controlled expiration. The BEAS2B response to mechanical load included altered mitochondrial activity, increased superoxide radical levels, NF-kappaB translocation, and release of interleukin-8. The response to strain was substantially modulated by the dynamics of the stimulation pattern. The rate of dynamic changes of the strain profile correlates with the degree of mechanical stress-induced cell response.

摘要

保护性机械通气旨在预防呼吸机所致肺损伤的同时保证充足的气体交换。一种新的方法侧重于机械通气的时间特性。我们假设时间机械应变特性可调节炎症信号。我们将各种时间特性的周期性应变施加于人支气管上皮细胞(BEAS2B)并评估其促炎反应。细胞接受正弦、矩形或三角形应变特性以及预应变矩形应变特性,预应变为最大应变的 0%、25%、50%或 75%,静态应变和类似于机械通气的应变特性,有无流量控制呼气。BEAS2B 对机械负荷的反应包括改变线粒体活性、增加超氧自由基水平、NF-κB 易位和白细胞介素-8 的释放。应变的反应受到刺激模式动力学的显著调节。应变特性的动态变化率与机械应激诱导的细胞反应程度相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/6fdc0dbf61fd/OMCL2019-2769761.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/20a4ccc4b5f5/OMCL2019-2769761.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/c96df9a14969/OMCL2019-2769761.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/893df1ce3dd8/OMCL2019-2769761.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/6fdc0dbf61fd/OMCL2019-2769761.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/20a4ccc4b5f5/OMCL2019-2769761.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/c96df9a14969/OMCL2019-2769761.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/893df1ce3dd8/OMCL2019-2769761.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf03/6607724/6fdc0dbf61fd/OMCL2019-2769761.004.jpg

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Characterizing cellular mechanical phenotypes with mechano-node-pore sensing.通过机械节点-孔隙传感来表征细胞力学表型。
用于研究不同肺通气方案及镇静剂作用的拉伸诱导性肺损伤模型
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Driving pressure and mechanical power: new targets for VILI prevention.驱动压力与机械功率:预防呼吸机所致肺损伤的新靶点
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