The effects of restraint stress on the neuropathogenesis of Theiler's virus infection: I. Acute disease
The effects of restraint stress on the neuropathogenesis of Theiler's virus infection: I. Acute disease
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DOI：
10.1006/brbi.2000.0598
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发表时间：
2001-09-01
影响因子：
15.1
通讯作者：
Welsh, CJR
中科院分区：
文献类型：
--
作者：
Campbell, T;Meagher, MW;Welsh, CJR
约束压力被发现对泰勒氏病毒感染的急性期有深远的影响。在感染泰勒氏病毒豆毒株的受限制的CBA小鼠中，观察到死亡率增加。此外，受限制的小鼠比感染/非受限制的小鼠发展出更高的CNS病毒滴度。感染和未感染的受抑小鼠均可观察到胸腺萎缩。在感染后7天，与非限制性感染小鼠相比，限制性感染小鼠的小胶质细胞增生、血管周围袖套和星形胶质细胞减少。束缚应激小鼠血液中淋巴细胞数量减少，中性粒细胞数量增加。这些改变的机制包括应激诱导的皮质酮，这会导致免疫抑制，减少炎症细胞在中枢神经系统的运输，从而增加病毒复制。(C)2001年学术出版社。
Restraint stress was found to have a profound effect on the acute phase of Theiler's virus infection. Increased mortality rates were observed in restrained CBA mice infected with the BeAn strain of Theiler's virus. In addition, restrained mice developed higher CNS viral titers than infected/nonrestrained mice. Thymic atrophy was observed in both infected and uninfected restrained mice. Decreased microgliosis, perivascular cuffing, and astrocytosis were observed in restrained mice compared to nonrestrained infected mice at 7 days postinfection. Restraint-stressed mice also developed decreased numbers of lymphocytes and increased numbers of neutrophils in the blood. The mechanism proposed for these alterations involves stress-induced corticosterone, which causes immunosuppression, decreased trafficking of inflammatory cells in the CNS, and, consequently, increased viral replication. (C) 2001 Academic Press.