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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice
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Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice

机译：弓形虫脑炎期间ADAMTS-13表达增加和细胞凋亡促进神经病理

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Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.
机译：弓形虫（T. gondii）是一种原生动物寄生虫，有可能在免疫受损的人和动物中引起严重的脑炎。我们以前的研究表明，弓形虫诱导高水平的一氧化氮（NO）产生，高的神经胶质激活（GFAP）和神经丝表达，从而导致中枢神经系统（CNS）的弓形虫性脑炎（TE）发生严重的神经变性。这项实验研究的目的是调查中枢神经系统中ADAMTS-13的表达和凋亡，并确定它们是否与弓形虫病的神经病理学和神经变性有关。感染ME49弓形虫的小鼠在免疫组织化学过程中，在慢性感染的发生和建立过程中，于10时在大脑组织中检测ADAMTS-13，胱天蛋白酶3，胱天蛋白酶8，胱天蛋白酶9，TNFR1和Bcl-xL的表达。感染后30天和60天。研究结果显示ADAMTS-13（P <0.005），caspase 3（P <0.05），caspase 8（P <0.05），caspase 9（P <0.005）和TNFR1（P <0.05）的表达水平大脑明显增加，而Bcl-xL表达减少（P <0.005）。我们研究中最突出的发现是，感染后10、30和60天ADAMTS-13显着增加，这可能在TE的血脑屏障完整性和CNS微环境的调节和保护中起重要作用。这些结果还表明，刚地弓形虫介导的细胞凋亡可能在TE过程中的神经变性和神经病理学机制中起关键作用和不同类型的作用。此外，ADAMTS-13的表达可能提供了进展的思路，对于诊断该疾病至关重要。据作者所知，这是第一个关于弓形虫感染小鼠中枢神经系统ADAMTS-13表达的报道。

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