Abstract
Neutrophil extracellular traps (NETs) are complexes of decondensed DNA fibers and antimicrobial peptides that are released by neutrophils and play important roles in many noninfectious diseases, such as cystic fibrosis, systemic lupus erythematosus, diabetes, and cancer. Recently, the formation of NETs has been detected in many central nervous system diseases and is thought to play different roles in the occurrence and development of these diseases. Researchers have detected NETs in acute ischemic stroke thrombi, and these NETs are thought to promote coagulation and thrombosis. NETs in ischemic brain parenchyma were identified as the cause of secondary nerve damage. High levels of NETs were also detected in grade IV glioma tissues, where NETs were involved in the proliferation and invasion of glioma cells by activating a signaling pathway. Extracellular web-like structures have also recently been observed in mice with traumatic brain injury (TBI), and it was hypothesized that NETs contribute to the development of edema after TBI. This article reviews the effect of NETs on multiple diseases that affect the CNS and explores their clinical application prospects.
Highlights
Neutrophils are critical components of the innate immune system and play important roles in central nervous system (CNS) diseases
An in vitro experiment showed that hemin, a heme-related molecule produced by the hemolysis of red blood cells, can activate neutrophils and induce morphological changes, degranulation, and neutrophil extracellular traps (NETs) release in neutrophils, which may explain how NETs are induced in intracerebral hemorrhage (ICH) [50]
There are growing evidences that NETs are present in many CNS diseases of different origins, in which they may play similar or different roles
Summary
Neutrophils are critical components of the innate immune system and play important roles in central nervous system (CNS) diseases. Researchers observed that accumulated neutrophils may discharge web-like chromatin structures modified with antimicrobial peptides named neutrophil extracellular traps (NETs), which destroy the BBB, lead to the subsequent damage of neurons, and are involved in many CNS diseases [12, 13]. In 2004, active neutrophils were found to release web-like structure consisting of decondensed (unwound) DNA decorated with histones and granular proteins, which were termed as NETs [14]. Crucial steps in the formation of NETs were described in early in vitro studies [17, 18] Neutrophil nuclei lose their characteristic lobular shape and swell after stimulation. As described later in this review, NETs are implicated in CNS diseases, including stroke, Alzheimer’s disease, and multiple sclerosis (MS)
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