Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis.

Swarup V; Ghosh J; Das S; Basu A

首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis.

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Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis.

机译：肿瘤坏死因子受体相关的死亡域介导的神经元死亡有助于日本脑炎的神经胶质活化和随后的神经炎症。

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While a number of studies have documented the importance of microglia in central nervous system (CNS) response to injury, infection and in disease state, little is known regarding how the neuronal death initiates the cascades of secondary neuroinflammation. We have exploited an experimental model of Japanese encephalitis to better understand how neuronal death following viral infection initiates microglial activation following Japanese encephalitis virus infection. We have earlier shown that the altered expression of tumor necrosis factor receptor-1 (TNFR-1) and TNFR associated death domain (TRADD) following Japanese encephalitis virus infection regulates the downstream apoptotic cascades. Here we have reported that silencing TRADD expression with small-interfering RNA reduced neuronal apoptosis and subsequent microglial and astroglial activation and release of various pro-inflammatory mediators. Our findings suggest that the engagement of TNFR-1 and TRADD following Japanese encephalitis virus infection plays a crucial role in glial activation also and influences the outcome of viral pathogenesis.

机译：虽然许多研究已证明小胶质细胞在中枢神经系统（CNS）对损伤，感染和疾病状态的反应中的重要性，但对于神经元死亡如何引发继发性神经炎症的级联知之甚少。我们已经利用日本脑炎的实验模型来更好地了解病毒感染后神经元死亡如何在日本脑炎病毒感染后引发小胶质细胞活化。我们先前已经表明，日本脑炎病毒感染后，肿瘤坏死因子受体1（TNFR-1）和TNFR相关死亡域（TRADD）的表达改变调节下游的凋亡级联反应。在这里我们已经报道了用小干扰RNA沉默TRADD表达减少了神经元凋亡以及随后的小胶质细胞和星形胶质细胞的激活以及各种促炎介质的释放。我们的发现表明，日本脑炎病毒感染后TNFR-1和TRADD的参与在神经胶质激活中也起着至关重要的作用，并影响病毒的发病机理。

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来源
《Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry》 |2008年第7期|共12页
作者
Swarup V; Ghosh J; Das S; Basu A;
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正文语种 eng
中图分类生物化学;
关键词
Cessation of life; Infection as complication of medical care; receptor; Microglia; 小神经胶质细胞; 肿瘤坏死因子;

机译：Cessation of life;Infection as complication of medical care;receptor;Microglia;小神经胶质细胞;肿瘤坏死因子;

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1. Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis. [J] . Swarup V, Ghosh J, Das S, Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry . 2008,第7期

机译：肿瘤坏死因子受体相关的死亡域介导的神经元死亡有助于日本脑炎的神经胶质活化和随后的神经炎症。
2. The epstein-barr virus oncogene product latent membrane protein 1 engages the tumor necrosis factor receptor-associated death domain protein to mediate B lymphocyte growth transformation and activate NF-κB [J] . Kenneth M.Izumi, Elliott D.Kieff Proceedings of the National Academy of Sciences of the United States of America . 1997,第23期

机译：EB病毒癌基因产物潜伏膜蛋白1与肿瘤坏死因子受体相关的死亡域蛋白结合，介导B淋巴细胞的生长转化并激活NF-κB
3. T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors. [J] . S Y Lee, C G Park, Y Choi The Journal of Experomental Medicine . 1996,第2期

机译：CD30胞质域介导的T细胞杂交瘤的T细胞受体依赖性细胞死亡与肿瘤坏死因子受体相关因子相关。
4. Sensitivity analysis of programmed cell death and implications for crosstalk phenomena during Tumor Necrosis Factor stimulation [C] . Thomas Eissing, Steffen Waldherr, Cedric Gondro, IEEE International Conference on Control Applications . 2006

机译：肿瘤坏死因子刺激期间编程细胞死亡的敏感性分析及串扰现象的影响
5. The Role of Tumor Necrosis Factor Alpha in Triggering Activated Cytolytic Natural Killer Cells Mediated Mitochondrial Dysfunction Leading to the Clinical Pathology of Pre-Eclampsia [D] . Jayaram, Aswathi. 2020

机译：肿瘤坏死因子α在触发活化的细胞溶解天然杀伤细胞中的作用介导的线粒体功能障碍导致预普利坦斯预混物的临床病理
6. The Epstein–Barr virus oncogene product latent membrane protein 1 engages the tumor necrosis factor receptor-associated death domain protein to mediate B lymphocyte growth transformation and activate NF-κB [O] . Kenneth M. Izumi, Elliott D. Kieff 1997

机译：爱泼斯坦-巴尔病毒癌基因产物潜伏膜蛋白1与肿瘤坏死因子受体相关的死亡域蛋白结合介导B淋巴细胞的生长转化并激活NF-κB
7. T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors [O] . 1996

机译：CD30胞质域与肿瘤坏死因子受体相关因子介导的T细胞杂交瘤的T细胞受体依赖性细胞死亡

Tumor necrosis factor receptor-associated death domain mediated neuronal death contributes to the glial activation and subsequent neuroinflammation in Japanese encephalitis.

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