West Nile virus encephalitis: sequential histopathological and immunological events in a murine model of infection
West Nile virus encephalitis: sequential histopathological and immunological events in a murine model of infection
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DOI：
10.1080/13550280601187185
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发表时间：
2007-01-01
影响因子：
3.2
通讯作者：
Kleiboeker, Steven B.
中科院分区：
文献类型：
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作者：
Garcia-Tapia, David;Hassett, Daniel E.;Kleiboeker, Steven B.
西尼罗河病毒（WNV）已成为北美人类和马脑炎的重要原因。尽管关于由这种黄病毒引起的疾病的发病机理以及关于针对它的免疫力有重要的知识，但是没有报道描述病理变化的顺序及其与感染西尼罗河病毒后大脑中的免疫应答的相关性。在这份报告中，作者描述了主要的组织病理学变化，以及细胞因子和趋化因子表达的变化，从WNV感染的C57 B1/6小鼠的大脑。在感染过程中，皮肤、脾脏和肾脏都是病毒进入大脑前的复制部位。在脑中，趋化因子单核细胞趋化蛋白（MCP）-5（CCL 12）、干扰素γ诱导蛋白10（IP-10; CXCL 10）和γ干扰素诱导的单核因子（; CXCL 9）先于干扰素γ的表达（IFN-γ）和肿瘤坏死因子α肿瘤坏死因子-α（TNF-α），其先前被认为是WNV脑炎的发病机制和免疫应答中的关键早期细胞因子。这些结果表明，趋化因子MCP-5，IP-10和MCP-10是脑炎症的重要触发因素，因为它们在WNV感染后早期上调。
West Nile virus (WNV) has emerged as an important cause of encephalitis in humans and horses in North America. Although there is significant knowledge about the pathogenesis of disease caused by this flavivirus and about the immunity against it, no reports exist describing the sequence of pathological changes and their correlation to the immune response in the brain following infection with WNV. In this report the authors describe the major histopathological changes, as well as changes in cytokine and chemokine expression, in brains from WNV-infected C57Bl/6 mice. During the course of infection skin, spleen and kidney were all sites of WNV replication before virus reached the brain. In brain, increased expression of the chemokines monocyte chemoattractant protein (MCP)-5 (CCL12), interferon gamma inducible protein 10 (IP-10; CXCL10), and monokine induced by gamma interferon ( MIG; CXCL9) preceded the expression of interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), which have previously been considered to be key early cytokines in the pathogenesis and immune response of WNV encephalitis. These results suggest that the chemokines MCP-5, IP-10, and MIG are important triggers of inflammation in brain due to their early up-regulation following WNV infection.