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On-line Access: 2022-07-06

Received: 2021-12-08

Revision Accepted: 2022-05-03

Crosschecked: 2022-07-06

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Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Xiaobo HU

https://orcid.org/0000-0001-7613-680X

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Journal of Zhejiang University SCIENCE B 2022 Vol.23 No.7 P.607-612

http://doi.org/10.1631/jzus.B2101029


PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis


Author(s):  Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU

Affiliation(s):  Department of Biochemistry and Molecular Biology, School of Basic Medicine, Hengyang Medical School, University of South China, Hengyang 421001, China; more

Corresponding email(s):   huxiaobo@foxmail.com

Key Words:  PFKL;NETosis;Neutrophil;NOX


Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU. PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis[J]. Journal of Zhejiang University Science B, 2022, 23(7): 607-612.

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author="Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU",
journal="Journal of Zhejiang University Science B",
volume="23",
number="7",
pages="607-612",
year="2022",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2101029"
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%T PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis
%A Zhaohui CAO
%A Di HUANG
%A Cifei TANG
%A Min ZENG
%A Xiaobo HU
%J Journal of Zhejiang University SCIENCE B
%V 23
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2101029

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T1 - PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis
A1 - Zhaohui CAO
A1 - Di HUANG
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A1 - Min ZENG
A1 - Xiaobo HU
J0 - Journal of Zhejiang University Science B
VL - 23
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SP - 607
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PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B2101029


Abstract: 
Neutrophils are predominant leukocytes in the circulation, which are essential for killing invading pathogens via the activation of effector responses and the production of reactive oxygen species (ROS), also named as "oxidative burst." When infected, activated neutrophils fight bacteria, fungi, and viruses through oxidative burst, phagocytosis, degranulation, and the production of neutrophil extracellular traps (NETs) in a neutrophil death process named as "NETosis" (Mutua and Gershwin, 2021). NETs, consisting of DNA fibers decorated with modified histones and numerous antimicrobial proteins from cytoplasmic granules and the nucleus, can either be beneficial or detrimental (Mutua and Gershwin, 2021). Several pathways can lead to this death process. In response to various stimuli, NETosis traps and clears pathogens, facilitating phagocytosis by other neutrophils and phagocytes. However, excessive NETosis often results in disease due to increasing the pro-inflammatory response and perpetuating the inflammatory condition (Hellebrekers et al., 2018; Hidalgo et al., 2019; Klopf et al., 2021). Accordingly, inhibiting aberrant NETosis may alleviate the severity of various autoimmune and inflammatory diseases.

磷酸果糖激酶L调节NADPH氧化酶-2依赖的氧化爆发和中性粒细胞的炎性死亡

曹朝晖1,2,黄狄1,2,唐慈妃1,2,曾敏1,2,胡小波1,2
1南华大学衡阳医学院生物化学与分子生物学教研室,中国衡阳市,421001
2南华大学衡阳医学院湖南省教育厅生态环境与重大疾病防治重点实验室,中国衡阳市,421001
概要:中性粒细胞胞外诱捕网(NETs),由活化的中性粒细胞释放的组蛋白和抗菌蛋白修饰的网状DNA纤维组成。中性粒细胞产生NETs,实现宿主防御作用,这一过程被称为中性粒细胞炎性死亡(NETosis)。NETosis是一把双刃剑,在应对各种外界刺激时,NETosis介导免疫反应,捕获和清除病原体,促进中性粒细胞和吞噬细胞的吞噬作用。然而,过度的NETosis增加炎症反应,持续炎症状态。因此,抑制异常NETosis的发生可以降低各种自身免疫性疾病和炎症性疾病的严重程度。磷酸果糖激酶L(PFKL)通过选择性激活中性粒细胞中的糖酵解通路,减少还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)产生,继而减少活性氧(ROS)的产生,抑制NETosis,为一些炎性疾病治疗提供新思路。

关键词:磷酸果糖激酶L(PFKL);中性粒细胞炎性死亡(NETosis);中性粒细胞;NADPH氧化酶(NOX)

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

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