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

Drew, Clifton P., Heller, Meera C., Mayo, Christie, Watson, Joie L., MacLachlan, N. James
Veterinary immunology and immunopathology 2010 v.136 no.3-4 pp. 292-296
cattle, cattle diseases, bluetongue, Bluetongue virus, infection, hemorrhage, pathogenesis, pathophysiology, immune response, monocytes, macrophages, macrophage activation, transcriptional activation, tumor necrosis factor-alpha, interleukins, nitric oxide synthase, interferons, pulmonary artery, endothelium, tissue tropism, in vitro studies, endothelial cells
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-α, IL-1β, 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.