克氏锥虫衍生神经营养因子:在神经修复和神经保护中的作用。

Marina V Chuenkova, Mercio Pereiraperrin
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引用次数: 8

摘要

一些感染克氏锥虫的患者会发展成慢性恰加斯病,而另一些患者则终生无症状。尽管控制疾病进展的病理机制尚不清楚,但周围神经系统退化和再生之间的平衡似乎导致了不同的临床结果。本文综述了与克氏绦虫反式唾液酸酶(又称寄生虫源性神经营养因子)诱导的宿主神经系统再生相关的宿主-寄生虫相互作用的某些新方面。PDNF在克氏绦虫感染中发挥多种作用,从免疫抑制到哺乳动物神经营养因子的功能模仿和细胞凋亡的抑制。PDNF与神经营养蛋白Trk受体的亲和力提供了细胞存活机制的持续激活,从而导致神经保护和神经元修复,抵抗细胞毒性损伤和增强神经新生。这种独特的pdnf诱导的再生反应可能会延长寄生虫在感染组织中的持久性,同时减少恰加斯病的神经病理学。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Trypanosoma cruzi-Derived Neurotrophic Factor: Role in Neural Repair and Neuroprotection.

Trypanosoma cruzi-Derived Neurotrophic Factor: Role in Neural Repair and Neuroprotection.

Some patients infected with the parasite Try-panosoma cruzi develop chronic Chagas' disease, while others remain asymptomatic for life. Although pathological mechanisms that govern disease progression remain unclear, the balance between degeneration and regeneration in the peripheral nervous system seems to contribute to the different clinical outcomes. This review focuses on certain new aspects of host-parasite interactions related to regeneration in the host nervous system induced by the trans-sialidase of T. cruzi, also known as a parasite-derived neurotrophic factor (PDNF). PDNF plays multiple roles in T. cruzi infection, ranging from immunosuppression to functional mimicry of mammalian neurotrophic factors and inhibition of apoptosis. PDNF affinity to neurotrophin Trk receptors provide sustained activation of cellular survival mechanisms resulting in neuroprotection and neuronal repair, resistance to cytotoxic insults and enhancement of neuritogenesis. Such unique PDNF-elicited regenerative responses likely prolong parasite persistence in infected tissues while reducing neuropathology in Chagas' disease.

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