PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis
Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU
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
huxiaobo@foxmail.com
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.
Key words: PFKL?NETosis?Neutrophil?NOX
Chinese Summary <21> 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