Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells.

Lei He,Min Cheng,Yanqin Fang,Jihui Lin,Wulong Liang,Yanming Zhang

doi:10.1186/s12917-014-0279-3

Abstract

BackgroundClassical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The swine vascular endothelial cell is a primary target cell for CSFV. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells.ResultsWe demonstrated that CSFV infection induced oxidative stress in swine umbilical vein endothelial cells (SUVECs), characterized by the induction of reactive oxygen species (ROS) production and the elevations of porcine antioxidant proteins thioredoxin (Trx), peroxiredoxin-6 (PRDX-6) and heme oxygenase-1 (HO-1) expression. Furthermore, cyclooxygenase-2 (COX-2), a pro-inflammatory protein related to oxidative stress, was up-regulated while anti-inflammatory protein peroxisome proliferator-activated receptor-γ (PPAR-γ), an important mediator in vascular functional regulation, was down-regulated in the CSFV infected cells. In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.ConclusionsOur results indicated that CSFV infection induced oxidative stress in SUVECs. These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

Highlights

Classical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia
The results of these findings have potentially important implications for the mechanism by which CSFV can alter intracellular events associated with the viral infection and the controlling this economically important animal disease
The level of reactive oxygen species (ROS) was increased with prolong cultured time as the level of ROS in swine umbilical vein endothelial cells (SUVECs) infected with CSFV at 72 h was significantly higher than 48 h and 24 h

Summary

Introduction

Classical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells. The infection of pigs with CSFV strains of high virulence such as shimen strain causes a severe acute disease with high mortality rate, characterized by haemorrhagic diathesis, leucopenia, thrombocytopenia and disseminated intravascular coagulation [3,4]. Mounting evidence has emphasized that vascular oxidative stress and increased production of ROS contribute to the mechanism of vascular dysfunction, while it was reported that blood vessel dysfunction plays an important role in the pathogenesis of CSFV [14]. It was reported to be decreased when oxidative stress and the aberrant expression of ROS occurred [16]

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