无菌性神经炎症及治疗干预策略

IF 2.6 Q3 IMMUNOLOGY International Journal of Inflammation Pub Date : 2017-01-03 DOI:10.1155/2017/8385961
Manoj Banjara, C. Ghosh
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引用次数: 60

摘要

无菌性神经炎症对正常的大脑发育和组织修复至关重要。然而,不受控制的神经炎症在各种疾病的发病过程中起着重要作用。内源性细胞内分子被称为损伤相关分子模式或警报或损伤信号,由活化或坏死细胞释放,被认为在启动免疫反应中起关键作用。无菌炎症反应发生在阿尔茨海默病(AD)、帕金森病(PD)、中风、出血、癫痫或创伤性脑损伤(TBI)中,造成了恶性循环的无节制炎症,导致神经退行性变。神经炎症是多种脑部疾病进展(如AD和PD)或继发性损伤发展(如中风、出血、应激和TBI)的关键机制。因此,它为治疗干预提供了机会,以防止进行性组织损伤和功能丧失。发展抗神经炎治疗的关键是尽量减少炎症的有害和神经毒性作用,同时促进有益和神经营养作用,从而为再生和修复创造理想的条件。本文概述了炎症如何参与主要非致病性神经炎症的发病机制,并讨论了神经胶质细胞对损伤信号的复杂反应。此外,还讨论了新兴的实验性抗神经炎药物治疗策略。
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Sterile Neuroinflammation and Strategies for Therapeutic Intervention
Sterile neuroinflammation is essential for the proper brain development and tissue repair. However, uncontrolled neuroinflammation plays a major role in the pathogenesis of various disease processes. The endogenous intracellular molecules so called damage-associated molecular patterns or alarmins or damage signals that are released by activated or necrotic cells are thought to play a crucial role in initiating an immune response. Sterile inflammatory response that occurs in Alzheimer's disease (AD), Parkinson's disease (PD), stroke, hemorrhage, epilepsy, or traumatic brain injury (TBI) creates a vicious cycle of unrestrained inflammation, driving progressive neurodegeneration. Neuroinflammation is a key mechanism in the progression (e.g., AD and PD) or secondary injury development (e.g., stroke, hemorrhage, stress, and TBI) of multiple brain conditions. Hence, it provides an opportunity for the therapeutic intervention to prevent progressive tissue damage and loss of function. The key for developing anti-neuroinflammatory treatment is to minimize the detrimental and neurotoxic effects of inflammation while promoting the beneficial and neurotropic effects, thereby creating ideal conditions for regeneration and repair. This review outlines how inflammation is involved in the pathogenesis of major nonpathogenic neuroinflammatory conditions and discusses the complex response of glial cells to damage signals. In addition, emerging experimental anti-neuroinflammatory drug treatment strategies are discussed.
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
16
审稿时长
16 weeks
期刊最新文献
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