Oligodendroglial pathology in canine distemper
Oligodendroglial pathology in canine distemper
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犬瘟热的少突胶质细胞病理学
DOI：
10.1007/s004010050767
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发表时间：
1997
影响因子：
12.7
通讯作者：
M. Vandevelde
中科院分区：
文献类型：
--
作者：
A. Zurbriggen;I. Schmid;H. Graber;M. Vandevelde
摘要 犬瘟热病毒（CDV）引起犬的多灶性脱髓鞘疾病。犬瘟热急性脱髓鞘的机制仍知之甚少。犬瘟热最初的脱髓鞘病变是由病毒直接引起的，因为脱髓鞘的发生与白质细胞中CDV复制之间存在明显的相关性。然而，几乎没有证据表明少突胶质细胞感染。这些细胞的变化已在体外和体内都有报道。体外研究表明，与星形胶质细胞和巨噬细胞等其他细胞相比，少突胶质细胞几乎不表达 CDV 蛋白。然而，我们可以证明这些细胞经历了 CDV RNA 转录的有限感染，并且这种现象与髓磷脂基因转录的下调相关。由于犬脑组织切片中缺乏可靠的少突胶质细胞标记技术，这些体外研究结果在体内的推广被掩盖了。在本研究中，我们将免疫组织化学与原位杂交相结合，检查脱髓鞘病变中的少突胶质细胞，并探讨体内少突胶质细胞感染的问题。我们可以证明 CDV 感染导致脱髓鞘病变中髓鞘质基因表达的大量下调，并且这种效应部分与少突胶质细胞的限制性感染相关。
Abstract Canine distemper virus (CDV) causes a multifocal demyelinating disease in dogs. The mechanism of acute demyelination in distemper is still poorly understood. The initial demyelinating lesion in distemper is directly virus induced, since there is a clear correlation between the occurrence of demyelination and CDV replication in the cells of the white matter. Yet, there is little evidence for oligodendroglial infection. Changes of these cells have been reported in vitro and in vivo. The in vitro studies showed that – in contrast to other cells such as astrocytes and macrophages – oligodendrocytes hardly express CDV protein. However, we could show that these cells underwent a restricted infection with transcription of CDV RNA and that this phenomenon correlated with down-regulation of myelin gene transcription. The extension of these in vitro findings in vivo was obscured by the lack of reliable oligodendrocyte labelling techniques in canine brain tissue sections. In this study we combined immunohistochemistry with in situ hybridization to examine oligodendrocytes in demyelinating lesions and to investigate the question of oligodendrocyte infection in vivo. We could demonstrate that CDV infection leads to massive down-regulation of myelin gene expression in demyelinating lesions and that this effect correlates in part with a restricted infection of oligodendrocytes.
影响因子：
2.7
作者：
COX, KH;DELEON, DV;ANGERER, RC
通讯作者：
ANGERER, RC