Viable neutrophils release mitochondrial DNA to form neutrophil extracellular traps

被引：772

作者：

Yousefi, S. ^{[1
]}

Mihalache, C. ^{[1
]}

Kozlowski, E. ^{[1
]}

Schmid, I. ^{[1
]}

Simon, H. U. ^{[1
]}

机构：

[1] Univ Bern, Inst Pharmacol, CH-3010 Bern, Switzerland

来源：

CELL DEATH AND DIFFERENTIATION | 2009年 / 16卷 / 11期

基金：

瑞士国家科学基金会;

关键词：

apoptosis; inflammation; mitochondrial DNA; neutrophils; neutrophil extracellular traps; APOPTOSIS; INFLAMMATION; INDUCTION;

D O I：

10.1038/cdd.2009.96

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Neutrophil extracellular traps (NETs) represent extracellular structures able to bind and kill microorganisms. It is believed that they are generated by neutrophils undergoing cell death, allowing these dying or dead cells to kill microbes. We show that, following priming with granulocyte/macrophage colony-stimulating factor (GM-CSF) and subsequent short-term toll-like receptor 4 (TLR4) or complement factor 5a (C5a) receptor stimulation, viable neutrophils are able to generate NETs. Strikingly, NETs formed by living cells contain mitochondrial, but no nuclear, DNA. Pharmacological or genetic approaches to block reactive oxygen species (ROS) production suggested that NET formation is ROS dependent. Moreover, neutrophil populations stimulated with GM-CSF and C5a showed increased survival compared with resting neutrophils, which did not generate NETs. In conclusion, mitochondrial DNA release by neutrophils and NET formation do not require neutrophil death and do also not limit the lifespan of these cells. Cell Death and Differentiation (2009) 16, 1438-1444; doi:10.1038/cdd.2009.96; published online 17 July 2009

引用

页码：1438 / 1444

页数：7

共 17 条

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