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

BMC Veterinary Research

Min Cheng²  Jihui Lin²  Wulong Liang²  Yanqin Fang²  Yanming Zhang²  Lei He¹ 

[1] Animal Disease and Public Security Academician Workstation of Henan province, The Key Lab of Animal Disease and Public security, Henan University of Science and Technology, Luoyang 471003, P.R. China;College of Veterinary Medicine, Northwest A & F University, Yangling 712100, Shaanxi, P.R. China

关键词: Inflammatory response;    Reactive oxygen species;    Antioxidant protein;    Oxidative stress;    Classical swine fever virus;   

Others  :  1103371
DOI  :  10.1186/s12917-014-0279-3

 received in 2014-07-11, accepted in 2014-11-11,  发布年份 2014

【 摘 要 】

Background

Classical 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.

Results

We 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.

Conclusions

Our 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.

【 授权许可】

   
2014 He et al.; licensee BioMed Central Ltd.

【 图 表 】

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