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Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

机译:神经炎症和感染:与神经血管单位功能障碍相关的分子机制

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摘要

Neuroinflammation is a complex inflammatory process in the central nervous system, which is sought to play an important defensive role against various pathogens, toxins or factors that induce neurodegeneration. The onset of neurodegenerative diseases and various microbial infections are counted as stimuli that can challenge the host immune system and trigger the development of neuroinflammation. The homeostatic nature of neuroinflammation is essential to maintain the neuroplasticity. Neuroinflammation is regulated by the activity of neuronal, glial, and endothelial cells within the neurovascular unit, which serves as a “platform” for the coordinated action of pro- and anti-inflammatory mechanisms. Production of inflammatory mediators (cytokines, chemokines, reactive oxygen species) by brain resident cells or cells migrating from the peripheral blood, results in the impairment of blood-brain barrier integrity, thereby further affecting the course of local inflammation. In this review, we analyzed the most recent data on the central nervous system inflammation and focused on major mechanisms of neurovascular unit dysfunction caused by neuroinflammation and infections.
机译:神经炎症是中枢神经系统中的一个复杂的炎症过程,旨在对各种引起神经变性的病原体,毒素或因子起重要的防御作用。神经退行性疾病和各种微生物感染的发作被视为可以挑战宿主免疫系统并触发神经炎症发展的刺激。神经炎症的体内稳态性质对于维持神经可塑性至关重要。神经炎症由神经血管单位内的神经元,神经胶质细胞和内皮细胞的活性来调节,这是促炎和消炎机制协同作用的“平台”。脑驻留细胞或从外周血迁移的细胞产生炎性介质(细胞因子,趋化因子,活性氧),导致血脑屏障完整性受损,从而进一步影响局部炎症过程。在这篇综述中,我们分析了有关中枢神经系统炎症的最新数据,重点研究了由神经炎症和感染引起的神经血管单位功能障碍的主要机制。

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