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PFKL,NOX2 依赖性氧化爆发和 NETosis 的新型调控节点。

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

机构信息

Department of Biochemistry and Molecular Biology, School of Basic Medicine, Hengyang Medical School, University of South China, Hengyang 421001, China.

The Key Laboratory of Ecological Environment and Critical Human Diseases Prevention of Hunan Province Department of Education, Hengyang Medical School, University of South China, Hengyang 421001, China.

出版信息

J Zhejiang Univ Sci B. 2022 Jul 15;23(7):607-612. doi: 10.1631/jzus.B2101029.

DOI:10.1631/jzus.B2101029
PMID:35794690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9264108/
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.

摘要

中性粒细胞是循环中主要的白细胞,通过激活效应反应和产生活性氧物种(ROS),也称为“氧化爆发”,对于杀死入侵的病原体至关重要。当被感染时,激活的中性粒细胞通过氧化爆发、吞噬作用、脱粒和产生中性粒细胞胞外陷阱(NETs)来对抗细菌、真菌和病毒,这个中性粒细胞死亡过程被称为“NETosis”(Mutua 和 Gershwin,2021)。NETs 由带有修饰组蛋白的 DNA 纤维和来自细胞质颗粒和细胞核的多种抗菌蛋白组成,可能有益也可能有害(Mutua 和 Gershwin,2021)。几种途径可以导致这种死亡过程。中性粒细胞在响应各种刺激时会通过 NETosis 捕获和清除病原体,促进其他中性粒细胞和吞噬细胞的吞噬作用。然而,由于过度 NETosis 会增加促炎反应并使炎症状态持续存在,因此通常会导致疾病(Hellebrekers 等人,2018 年;Hidalgo 等人,2019 年;Klopf 等人,2021 年)。因此,抑制异常的 NETosis 可能会减轻各种自身免疫和炎症性疾病的严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ff4/9264108/8685d6e94700/JZhejiangUnivSciB-23-7-607-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ff4/9264108/8685d6e94700/JZhejiangUnivSciB-23-7-607-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ff4/9264108/8685d6e94700/JZhejiangUnivSciB-23-7-607-g001.jpg

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