Abstract
BackgroundDysfunction of endothelial cells and vascular system is one of the most important pathological changes of porcine circovirus disease (PCVD) caused by porcine circovirus type 2 (PCV2). PCV2-infected endothelial cells can upregulate the production of endothelial-derived IL-8, which can inhibit the maturation of dendritic cells. Endothelial-derived IL-8 has different structural and biological characteristics compared with monocyte-derived IL-8. However, the mechanism of endothelial-derived IL-8 production is still unclear.ResultsKey molecules of RIG-I-like signaling pathway RIG-I, MDA-5, MAVS and a key molecule of JNK signaling pathway c-Jun in PCV2-infected porcine iliac artery endothelial cells (PIECs) were upregulated significantly detected with quantitative PCR, Western blot and fluorescence confocal microscopy, while no significant changes were found in NF-κB signaling pathway. Meanwhile, the expression of endothelial-derived IL-8 was downregulated after RIG-I, MDA-5, or MAVS genes in PIECs were knocked down and PIECs were treated by JNK inhibitor.ConclusionsPCV2 can activate RIG-I/MDA-5/MAVS/JNK signaling pathway to induce the production of endothelial-derived IL-8 in PIECs, which provides an insight into the further study of endothelial dysfunction and vascular system disorder caused by PCV2.
Highlights
Dysfunction of endothelial cells and vascular system is one of the most important pathological changes of porcine circovirus disease (PCVD) caused by porcine circovirus type 2 (PCV2)
PCV2 can activate retinoic acid-inducible gene I (RIG-I)/melanoma differentiation-associated gene-5 (MDA-5)/mitochondrial antiviral signaling protein (MAVS)/JNK signaling pathway to induce the production of endothelialderived IL-8 in porcine iliac artery endothelial cells (PIECs), which provides an insight into the further study of endothelial dysfunction and vascular system disorder caused by PCV2
Western blot showed that the protein expression levels of RIG-I, MDA-5 and MAVS were significantly upregulated in PCV2-PIECs group compared with the PIECs group (P < 0.01) (Fig. 1d and Fig. 2)
Summary
Dysfunction of endothelial cells and vascular system is one of the most important pathological changes of porcine circovirus disease (PCVD) caused by porcine circovirus type 2 (PCV2). The mechanism of endothelial-derived IL-8 production is still unclear. Epithelial IL-8 can be induced by parainfluenza virus type 1 via phosphorylation (p38) of the mitogenactivated protein kinase (p38-MAPKs) signaling pathway [8]. Monocyte-derived IL-8 can be induced by PCV2 via the TLR2/MyD88/NF-κB signaling pathway in porcine alveolar macrophages [9]. It is reported that PCV2 can induce IFN-β production via the RIG-1/ MDA-5/MAVS/IRF signaling pathway in PK-15 cell [15]. Classical swine fever virus can induce the production of IL-8 and other proinflammatory cytokines via the RIG-I/MDA-5 pathway [16, 17]. Whether the mechanism of endothelial-derived IL-8 production is consistent to that of other cell-derived IL-8 is still unknown
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