Endothelial IL-8 induced by porcine circovirus type 2 affects dendritic cell maturation and antigen-presenting function

Shiyu Liu,Jianfang Wang,Huanrong Li,Defeng Cui,Shuanghai Zhou,Jinzeng Qiao,Qiuming Li,Kewei Gu

doi:10.1186/s12985-019-1256-z

Shiyu Liu, Jianfang Wang + Show 6 more

Open Access

https://doi.org/10.1186/s12985-019-1256-z

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Journal: Virology journal	Publication Date: Dec 1, 2019
Citations: 9	License type: open-access

Affiliation: Beijing University of Agriculture

Abstract

BackgroundPorcine circovirus (PCV) disease caused by PCV type 2 (PCV2) is mainly attributed to immunosuppression and immune damage. PCV2 can infect vascular endothelial cells and induce high expression of endothelial IL-8. Dendritic cells (DCs), as professional antigen-presenting cells, can not only present antigens but also activate naïve T-cells, causing an immune response.MethodsTo demonstrate whether endothelial IL-8 is the main factor inhibiting the maturation and related functions of dendritic cells during PCV2 infection, monocyte-derived DCs (MoDCs) and porcine iliac artery endothelial cells (PIECs) processed by different methods were co-cultured in two ways. Flow cytometry, molecular probe labeling, fluorescence quantitative PCR, and the MTS assay were used to detect the changes in related functions and molecules of MoDCs.ResultsCompared to those in the PIEC-DC group, the endothelial IL-8 upregulation co-culture group showed significantly lower double-positive rates for CD80/86 and MHC-II of MoDCs and significantly increased endocytosis of MoDCs. Meanwhile, the adhesion rate and average fluorescence intensity of MoDCs were significantly downregulated in migration and adhesion experiments. Furthermore, the MHC-I and LAMP7 mRNA levels in MoDCs and the proliferation of MoDC-stimulated T-cells were markedly reduced. However, the changes in MoDCs of the endothelial IL-8 downregulation co-culture group were the opposite.ConclusionsPCV2-induced endothelial IL-8 reduces the adhesion and migration ability of MoDCs, resulting in a decreased maturation rate of MoDCs, and further inhibits antigen presentation by DCs. These results may explain the immunosuppressive mechanism of PCV2 from the perspective of the interaction between endothelial cells and DCs in vitro.

Highlights

Porcine circovirus (PCV) disease caused by PCV type 2 (PCV2) is mainly attributed to immunosuppression and immune damage
Endothelial IL-8 induced by PCV2 inhibited the maturation of monocyte-derived DCs (MoDCs) As seen in Fig. 1A, more than 90% of MoDCs were positive for both CD1a and SWC3a, which indicated MoDCs had been induced successfully
Using MoDCs co-cultured with porcine iliac artery endothelial cells (PIECs) processed by different methods, we found that the PCV2-induced endothelial IL-8 could affect MoDC maturation by inhibiting their adhesion and migration ability

Summary

Introduction

Porcine circovirus (PCV) disease caused by PCV type 2 (PCV2) is mainly attributed to immunosuppression and immune damage. DCs can deliver antigen peptides to CD4+ Th cells through binding of the major histocompatibility complex (MHC)-II to antigen peptides, and to CD8+ Tc cells by binding of MHC-I class molecules to antigen peptides [12], which play an important role in the body’s antiviral immunity. Some viruses, such as Herpes virus [13], influenza virus [14], and human immunodeficiency virus [15], can evade or delay immune responses by disrupting DC function [16, 17]

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