Protein expression profile of mast cells in response to recombinant VP1-VP4 of foot-and-mouth disease virus.

Yan Wang; Shasha Zhang; Lei Wang; Xuefang Liu; En Zhang; Na LI; Yunhuan Gao; Yiming Zhang; Limin LI; Jiaxin Wang

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Protein expression profile of mast cells in response to recombinant VP1-VP4 of foot-and-mouth disease virus.

Author: Yan WANG ¹ ; Shasha ZHANG ¹ ; Lei WANG ¹ ; Xuefang LIU ¹ ; En ZHANG ¹ ; Na LI ¹ ; Yunhuan GAO ¹ ; Yiming ZHANG ¹ ; Limin LI ¹ ; Jiaxin WANG ¹
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1. Laboratory of Immunology, College of Veterinary Medicine, Agricultural University of Hebei, Baoding 071000, Hebei, China.
Publication Type:Journal Article
Keywords: differential expression; foot-and-mouth disease virus; innate immunity; mannose receptor; mast cells
MeSH: Animals; Capsid Proteins; immunology; Cells, Cultured; Cytokines; immunology; Enzyme-Linked Immunosorbent Assay; Foot-and-Mouth Disease; Foot-and-Mouth Disease Virus; Interleukins; immunology; Mast Cells; immunology; Mice; Proteome; immunology; Recombinant Proteins; immunology; Viral Structural Proteins; immunology
From: Chinese Journal of Biotechnology 2016;32(9):1194-1203
CountryChina
Language:Chinese
Abstract: To reveal the innate immunity of mast cells against recombinant VP1-VP4 protein of foot-and-mouth disease virus (FMDV), mouse peritoneal mast cells (PMCs) were pulsed with recombinant VP1-VP4 protein. The supernatants harvested from PMCs cultures were applied to the high throughput ELISA array. Our results show that the expression levels of CCL19, L-selectin, CCL17, and TNF alpha released from PMCs pulsed with recombinant VP1-VP4 were significantly down-regulated compared with PMCs alone (P<0.001). Surprisingly, in comparison with PMCs alone, the expression levels of CCL19, IL-15, IL-9, G-CSF, and Galectin-1 in PMCs with the mannose receptor (MR) inhibitor were significantly up-regulated (Plt;0.01), and the expression level of IL-10 was also remarkably up-regulated (Plt;0.05). Importantly, the protein expression levels in PMCs treated with MR inhibitor were higher than PMCs pulsed with VP1-VP4, including IL-10, IL-17, CCL20, IL-15, IL-9, L-selectin, CCL17, TNF alpha, and CCL19 (Plt;0.01) as well as CCL21, and G-CSF (Plt;0.05). Differential expression analysis in bioinformatics shows that both L-selectin and CCL17 were recognized as differentially expressed protein molecules (Log2(ratio)≤-1) when compared with PMCs alone. Furthermore, the up-regulation of the expression levels of CCL20, CCL19, L-selectin, and IL-15 in PMCs treated with MR inhibitor was defined as differential expression (Log2(ratio)≥1). These data indicate that PMCs are capable of secreting CCL19, L-selectin, CCL17, and TNF alpha spontaneously and the recombinant VP1-VP4 has an inhibitive potential to PMCs during their performance of innate immune response. Given the protein expression levels from PMCs pre-treated with MR inhibitor were significantly increased, it can be deduced that immunosuppression of FMDV is presumably initiated by the VP1 recognition of MR on mast cells.