Nicotine induces neutrophil extracellular traps
Nicotine induces neutrophil extracellular traps
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DOI：
10.1189/jlb.3ab0815-379rr
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发表时间：
2016-11-01
影响因子：
5.5
通讯作者：
Urban, Constantin F.
中科院分区：
文献类型：
--
作者：
Hosseinzadeh, Ava;Thompson, Paul R.;Urban, Constantin F.
NET用于诱捕和杀死微生物病原体。然而，NET同时也会导致组织损伤和过度炎症。尼古丁是一种主要的有毒物质，与炎症性疾病的加重有关。目前的研究旨在调查烟草和电子烟的成瘾成分尼古丁在触发NET形成中的作用。我们报告尼古丁以剂量依赖性方式诱导中性粒细胞释放NET。尼古丁诱导的NET形成通过尼古丁乙酰胆碱受体介导，依赖于Akt和PAD 4激活，但不依赖于Nox 2，如Nox 2的药理学抑制和Nox 2缺陷小鼠中性粒细胞的使用所证明的。这些发现表明，尼古丁诱导NET，这反过来可能有助于吸烟相关疾病。
NETs serve to ensnare and kill microbial pathogens. However, NETs can at the same time contribute to tissue damage and excessive inflammation. Nicotine is a major toxic agent and has been associated with exacerbated inflammatory diseases. The current study aimed at investigating the role of nicotine, the addictive component of tobacco and electronic cigarettes, on triggering NET formation. We report that nicotine induces neutrophils to release NETs in a dose-dependent manner. Nicotine-induced NET formation is mediated via nicotine acetylcholine receptors, depends on Akt and PAD4 activation, but is Nox2-independent, as demonstrated by pharmacological inhibition of Nox2 and by use of Nox2-deficient mouse neutrophils. These findings demonstrate that nicotine induces NETs, which may in turn contribute to smoking-related diseases.