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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Accumulation of the proinflammatory cytokine endothelial-monocyte-activating polypeptide II in ramified microglial cells in brains of Borna virus infected Lewis rats.
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Accumulation of the proinflammatory cytokine endothelial-monocyte-activating polypeptide II in ramified microglial cells in brains of Borna virus infected Lewis rats.

机译:感染博尔纳病毒的Lewis大鼠大脑中分枝的小胶质细胞中促炎性细胞因子内皮单核细胞激活多肽II的积累。

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摘要

Borna disease virus (BDV) infection of adult Lewis rats induces a severe and often fatal neurologic disease characterized by a massive mononuclear meningo-encephalitis, and activation of microglial cells. Therefore, we analyzed expression of endothelial monocyte activating polypeptide II (EMAP II) by immunohistology as a marker for activation of microglial cells in BDV infected rat brains. EMAP II is a chemotactic peptide, inducing activation of macrophages and endothelial cells, and is considered a proinflammatory mediator of the innate immune system. An up to 30-fold increase in numbers of EMAP II+ microglial cells and a massive expression by infiltrating macrophages at perivascular inflammatory foci was observed in infected brains, with a maximum on day 25 after infection. These results provide evidence that EMAP II contributes to immune responses in inflammatory processes caused by viral infections.
机译:成年Lewis大鼠的Borna病病毒(BDV)感染会引起严重且往往是致命的神经系统疾病,其特征是大量单核脑膜脑炎和小胶质细胞活化。因此,我们通过免疫组织学分析了内皮单核细胞活化多肽II(EMAP II)的表达,作为BDV感染大鼠脑中小胶质细胞活化的标志。 EMAP II是一种趋化肽,可诱导巨噬细胞和内皮细胞激活,并被认为是先天免疫系统的促炎介质。在受感染的大脑中,观察到EMAP II +小胶质细胞的数量增加了多达30倍,并且通过浸润在血管周围炎性灶处的巨噬细胞而大量表达,在感染后第25天达到最大值。这些结果提供了证据,EMAP II有助于由病毒感染引起的炎症过程中的免疫反应。

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