Neutrophil Extracellular Traps Are Pathogenic in Ventilator-Induced Lung Injury and Partially Dependent on TLR4

被引:37
作者
Li, Haosi [1 ]
Pan, Pinhua [1 ]
Su, Xiaoli [1 ]
Liu, Shuai [1 ]
Zhang, Lemeng [2 ,3 ]
Wu, Dongdong [1 ]
Li, Haitao [1 ]
Dai, Minhui [1 ]
Li, Yi [1 ]
Hu, Chengping [1 ]
Chen, Jie [1 ]
机构
[1] Cent South Univ, Xiangya Hosp, Dept Pulm & Crit Care Med, Changsha 410008, Hunan, Peoples R China
[2] Cent South Univ, Hunan Canc Hosp, Dept Thorac Med, Changsha 410013, Hunan, Peoples R China
[3] Cent South Univ, Xiangya Sch Med, Affiliated Canc Hosp, Changsha 410013, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
TIDAL-VOLUME VENTILATION; MECHANICAL VENTILATION; RECEPTOR; ACTIVATION; CONTRIBUTES; EXPRESSION; STRATEGIES; MEDIATORS; HISTONES; CAPTURE;
D O I
10.1155/2017/8272504
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The pathogenesis of ventilator-induced lung injury (VILI) is associated with neutrophils. Neutrophils release neutrophil extracellular traps (NETs), which are composed of DNA and granular proteins. However, the role of NETs in VILI remains incompletely understood. Normal saline and deoxyribonuclease (DNase) were used to study the role of NETs in VILI. To further determine the role of Toll-like receptor 4 (TLR4) in NETosis, we evaluated the lung injury and NET formation in TLR4 knockout mice and wild-type mice that were mechanically ventilated. Some measures of lung injury and the NETs markers were significantly increased in the VILI group. DNase treatment markedly reduced NETs markers and lung injury. After high-tidal mechanical ventilation, the NETs markers in the TLR4 KO mice were significantly lower than in the WT mice. These data suggest that NETs are generated in VILI and pathogenic in a mouse model of VILI, and their formation is partially dependent on TLR4.
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页数:13
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