克氏锥虫诱导的中枢神经系统改变:从炎症细胞的进入到潜在的认知和精神异常

A. A. Silva, G. Pereira, A. S. Souza, Rafael Rodrigues Silva, M. Rocha, J. Lannes-Vieira
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引用次数: 30

摘要

克氏锥虫是一种原生动物寄生虫,是恰加斯病的病原体,能够诱发脑膜脑炎。在免疫正常的克氏锥虫感染患者中观察到的从急性到慢性心肌炎的独立进展,中枢神经系统(CNS)炎症在急性感染期间自行消退。相反,在慢性感染免疫功能低下的Cha- gas病患者中,中枢神经系统是再激活的主要部位,可导致严重且经常致命的脑膜原-脑炎。在发现恰加斯病一百多年后,关于克鲁兹锥虫引起的脑膜脑炎的诱导和解决的分子机制的许多问题仍然没有答案。对重现T. cruzi引起的中枢神经系统炎症的关键方面的小鼠模型的研究不仅阐明了这些问题中的一些,而且还提出了其他问题。在这里,我们在当前文献的背景下讨论了我们的结果,质疑炎症和寄生虫引起的中枢神经系统改变是否参与了克氏锥虫感染期间观察到的行为异常。
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Trypanosoma cruzi-Induced Central Nervous System Alterations: From the Entry of Inflammatory Cells to Potential Cognitive and Psychiatric Abnormalities
Trypanosoma cruzi, a protozoan parasite and the causative agent of Chagas disease, is capable of inducing meningoencephalitis. Independent of the progression from acute to chronic myocarditis observed in immunocompetent T. cruzi-infected patients, inflammation of the central ner- vous system (CNS) self-resolves during acute infection. In contrast, in chronically infected immunocompromised Cha- gas disease patients, the CNS is a major site of reactivation, which can lead to severe and frequently fatal meningoen- cephalitis. More than one hundred years after the discovery of Chagas disease, many questions concerning the molecu- lar mechanisms involved in the induction and resolution of T. cruzi-provoked meningoencephalitis remain unanswered. The study of murine models that reproduce crucial aspects of T. cruzi-elicited CNS inflammation has not only shed light on some of these questions, but it has also raised additional ones. Here, we discuss our results in the context of the cur- rent literature, questioning the involvement of CNS alter- ations caused by the inflammation and parasite in the behav- ioral abnormalities observed during T. cruzi infection.
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