Differential chemokine induction by the mouse adenovirus type-1 in the central nervous system of susceptible and resistant strains of mice

被引:52
作者
Charles, PC
Chen, X
Horwitz, MS
Brosnan, CF
机构
[1] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA
[2] Albert Einstein Coll Med, Dept Immunol & Microbiol, Bronx, NY 10461 USA
[3] Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA
[4] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA
关键词
adenovirus; encephalopathy; chemokines; chemokine receptors;
D O I
10.3109/13550289909029746
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mouse adenovirus-type 1 (MAV-1) has recently been shown to cause a fatal hemorrhagic encephalopathy in certain strains of mice whereas other strains are resistant, Morbidity is associated with a productive infection of cerebrovascular endothelial cells, resulting in necrosis of the vasculature, infarction, hemorrhage and death within 4 - 6 days. Previous studies were not able to define a role for the innate or acquired immune response. In the current study we have addressed the effect of MAV-1 on chemokine and chemokine receptor expression in the central nervous system (CNS) and spleen of susceptible (C57BL/6) and resistant (BALB/c) strains of mice. Intra-peritoneal infection with MAV-1 in C57BL/6 animals resulted in early and prominent induction of IP-10/crg-2 in the spleen and CNS. Increased expression of MCP-1, MIP-1 alpha, MIP-1 beta and RANTES was also noted in the CNS of MAV-1-infected C57BL/6 animals commencing around 72 h post-infection, In contrast, chemokine expression in BALB/c animals was more restricted with prominent upregulation only of MIP-2 in the CNS. In situ hybridization identified the vascular endothelium and CNS glia as the principal site of IP-10/crg-2 production in the C57BL/6 animals. The chemokine receptors CCR1-5 were upregulated in the CNS of both strains of mice. These data show that productive infection of the CNS with MAV-1 leads to the upregulation of a characteristic pattern of chemokines and their receptors, which may point to a role for these factors in disease pathogenesis.
引用
收藏
页码:55 / 64
页数:10
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