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外周炎症对多发性硬化进展的影响:来自临床和实验动物模型的证据。

Influence of Peripheral inflammation on the progression of multiple sclerosis: evidence from the clinic and experimental animal models.

机构信息

Leloir Institute Foundation, Institute for Biochemical Investigations, CONICET, Buenos Aires, Argentina.

出版信息

Mol Cell Neurosci. 2013 Mar;53:6-13. doi: 10.1016/j.mcn.2012.06.004. Epub 2012 Jul 4.

DOI:10.1016/j.mcn.2012.06.004
PMID:22771835
Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease characterized by demyelination, remyelination and loss of functions. Even though its etiology is unknown viral, genetic and environmental factors are considered triggers of the disease. MS shows a heterogeneous clinical course, but most patients exhibit exacerbations and remissions from the onset, eventually leading to secondary progressive multiple sclerosis. Systemic inflammatory events are known to signal into the central nervous system (CNS), and can induce a general response known as sickness behavior. Several research papers have demonstrated that a peripheral stimulus can induce the synthesis of cytokines in the brain. In different neurodegenerative diseases peripheral inflammation generates exacerbation to ongoing damage in the brain. In MS, relapsing and remitting episodes are unpredictable; however, peripheral inflammation may exacerbate these events. Clinical studies revealed an association between infections and relapses, which may lead to the worsening of neurological damage. A similar scenario was described in MS animal models demonstrating that peripheral inflammation recrudesced a central ongoing demyelinating lesion. In this paper, we reviewed the existing data on the inflammatory component of MS, with special attention on the effect of peripheral infections in the etiology and progression of MS and its effect on the relapsing and remitting episodes. We also analyzed data concerning the effect of peripheral inflammatory events in MS experimental animal models. This article is part of a Special Issue entitled 'Neuroinflammation in neurodegeneration and neurodysfunction'.

摘要

多发性硬化症(MS)是一种慢性炎症性疾病,其特征是脱髓鞘、髓鞘再生和功能丧失。尽管其病因尚不清楚,但病毒、遗传和环境因素被认为是该病的诱因。MS 表现出异质性的临床病程,但大多数患者从发病开始就出现恶化和缓解,最终导致继发性进行性多发性硬化症。已知全身炎症事件会向中枢神经系统(CNS)发出信号,并可引发一种称为疾病行为的一般反应。一些研究论文已经证明,外周刺激可以诱导大脑中的细胞因子合成。在不同的神经退行性疾病中,外周炎症会加剧大脑中的持续损伤。在 MS 中,复发和缓解期是不可预测的;然而,外周炎症可能会加重这些事件。临床研究表明感染与复发之间存在关联,这可能导致神经损伤恶化。在 MS 动物模型中描述了类似的情况,表明外周炎症使中枢持续脱髓鞘病变恶化。在本文中,我们综述了 MS 炎症成分的现有数据,特别关注外周感染在 MS 的病因和进展中的作用及其对复发和缓解期的影响。我们还分析了关于外周炎症事件在 MS 实验动物模型中的作用的数据。本文是题为“神经退行性和神经功能障碍中的神经炎症”的特刊的一部分。

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