Upregulation of COX-2 and CGRP expression in resident cells of the Borna disease virus-infected brain is dependent upon inflammation

被引:33
作者
Röhrenbeck, AM
Bette, M
Hooper, DC
Nyberg, F
Eiden, LE
Dietzschold, B
Weihe, E
机构
[1] Univ Marburg, Inst Anat & Cell Biol, D-35032 Marburg, Germany
[2] Thomas Jefferson Univ, Dept Microbiol & Immunol, Ctr Neurovirol, Philadelphia, PA 19107 USA
[3] Uppsala Univ, Dept Pharmaceut Sci, Ctr Biomed, S-75105 Uppsala, Sweden
[4] NIMH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA
关键词
Borna disease virus; cyclooxygenase; prostaglandin; calcitonin gene-related peptide; neuropeptide; neocortex; hippocampus; macrophage/microglia; endothelium; encephalitis; dexamethasone; neuroimmunology; neurotoxicity; neuroprotection;
D O I
10.1006/nbdi.1998.0225
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Infection of immunocompetent adult rats with Borna disease virus (BDV) causes severe encephalitis and neural dysfunction. The expression of COX-2 and CORP, genes previously shown to be implicated in CNS disease and peripheral inflammation, was dramatically upregulated in the cortical neurons of acutely BDV-infected rats. Neuronal COX-2 and CGRP upregulation was predominantly seen in brain areas where ED1-positive macrophages/microglia accumulated. In addition, COX-2 expression was strongly induced in brain endothelial cells and the number of COX-2 immunoreactive microglial cells was increased. In contrast, despite increased expression of viral antigens, neither COX-2 nor CGRP expression was altered in the CNS of BDV-infected rats treated with dexamethasone, or tolerant to BDV. Thus, increased CGRP and COX-2 expression in the BDV-infected brain is the result of the inflammatory response and likely to be involved in the pathogenesis of virus-induced encephalitis. (C) Press Academic Press.
引用
收藏
页码:15 / 34
页数:20
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