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蓝舌病病毒感染可激活牛单核细胞衍生的巨噬细胞和肺动脉内皮细胞。

Bluetongue virus infection activates bovine monocyte-derived macrophages and pulmonary artery endothelial cells.

作者信息

Drew Clifton P, Heller Meera C, Mayo Christie, Watson Joie L, Maclachlan N James

机构信息

Department of Veterinary Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.

出版信息

Vet Immunol Immunopathol. 2010 Aug 15;136(3-4):292-6. doi: 10.1016/j.vetimm.2010.03.006. Epub 2010 Mar 10.

DOI:10.1016/j.vetimm.2010.03.006
PMID:20359752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2902619/
Abstract

Bluetongue virus (BTV) is the cause of bluetongue (BT), an emerging, arthropod-transmitted disease of ungulates. The cellular tropism of BTV in ruminants includes macrophages, dendritic cells and endothelial cells (ECs), and fulminant infection is characterized by lesions consistent with those of so-called viral hemorrhagic fevers. Specifically, BT is characterized by vascular injury with hemorrhage, tissue infarction and widespread edema. To further investigate the pathogenesis of vascular injury in BT, we evaluated the responses of cultured bovine pulmonary artery EC (bPAEC) and monocyte-derived macrophages (bMDM) to BTV infection by measuring transcript levels of genes encoding molecules important in mediating EC activation and/or endothelial barrier dysregulation. The data confirm that BTV infection of bPAEC resulted in increased transcription of genes encoding chemokine ligand 2 (CCL2) and E-selectin, and BTV infection of bMDM resulted in increased transcription of genes encoding TNF-alpha, IL-1beta, IL-8, and inducible nitric oxide synthase (iNOS). The data from these in vitro studies provide further evidence that cytokines and other vasoactive substances produced in macrophages potentially contribute to vascular injury in BTV-infected ruminants, along with direct effects of the virus itself on ECs.

摘要

蓝舌病病毒(BTV)是蓝舌病(BT)的病原体,蓝舌病是一种新出现的、由节肢动物传播的有蹄类动物疾病。BTV在反刍动物中的细胞嗜性包括巨噬细胞、树突状细胞和内皮细胞(ECs),暴发性感染的特征是出现与所谓病毒性出血热一致的病变。具体而言,蓝舌病的特征是血管损伤伴出血、组织梗死和广泛水肿。为了进一步研究蓝舌病中血管损伤的发病机制,我们通过测量编码介导EC激活和/或内皮屏障失调的重要分子的基因转录水平,评估了培养的牛肺动脉内皮细胞(bPAEC)和单核细胞衍生巨噬细胞(bMDM)对BTV感染的反应。数据证实,BTV感染bPAEC导致编码趋化因子配体2(CCL2)和E-选择素的基因转录增加,BTV感染bMDM导致编码肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-8和诱导型一氧化氮合酶(iNOS)的基因转录增加。这些体外研究的数据提供了进一步的证据,表明巨噬细胞产生的细胞因子和其他血管活性物质可能导致BTV感染的反刍动物出现血管损伤,同时病毒本身也对内皮细胞有直接影响。

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Antiviral responses of bluetongue virus-inoculated bovine fetuses and their dams.接种蓝舌病毒的牛胎儿及其母体的抗病毒反应。
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