cGAS/STING signaling pathways induces the secretion of type Ⅰ interferon in porcine alveolar macrophages infected with porcine circovirus type 2.
- Author:
Hongbo CHEN
1
;
Feng LI
1
;
Wenyan LAI
1
;
Yuhao FANG
1
;
Mingyong JIANG
1
;
Dianning DUAN
1
;
Xiaoyan YANG
1
Author Information
- Publication Type:Journal Article
- Keywords: innate immune signaling pathway; porcine alveolar macrophages; porcine circovirus type 2; type Ⅰ interferon
- MeSH: Animals; Cells, Cultured; Circovirus; Interferon Type I/genetics*; Macrophages, Alveolar/virology*; Membrane Proteins/metabolism*; Nucleotidyltransferases/metabolism*; Signal Transduction; Swine
- From: Chinese Journal of Biotechnology 2021;37(9):3201-3210
- CountryChina
- Language:Chinese
- Abstract: In order to study the signal pathway secreting type Ⅰ interferon in porcine alveolar macrophages (PAMs) infected with porcine circovirus type 2 (PCV2), the protein and the mRNA expression levels of cGAS/STING pathways were analyzed by ELISA, Western blotting and quantitative reverse transcriptase PCR in PAMs infected with PCV2. In addition, the roles of cGAS, STING, TBK1 and NF-κB/P65 in the generation of type I interferon (IFN-I) from PAMs were analyzed by using the cGAS and STING specific siRNA, inhibitors BX795 and BAY 11-7082. The results showed that the expression levels of IFN-I increased significantly at 48 h after infection with PCV2 (P<0.05), the mRNA expression levels of cGAS increased significantly at 48 h and 72 h after infection (P<0.01), the mRNA expression levels of STING increased significantly at 72 h after infection (P<0.01), and the mRNA expression levels of TBK1 and IRF3 increased at 48 h after infection (P<0.01). The protein expression levels of STING, TBK1 and IRF3 in PAMs infected with PCV2 were increased, the content of NF-κB/p65 was decreased, and the nuclear entry of NF-κB/p65 and IRF3 was promoted. After knocking down cGAS or STING expression by siRNA, the expression level of IFN-I was significantly decreased after PCV2 infection for 48 h (P<0.01). BX795 and BAY 11-7082 inhibitors were used to inhibit the expression of IRF3 and NF-κB, the concentration of IFN-I in BX795-treated group was significantly reduced than that of the PCV2 group (P<0.01), while no significant difference was observed between the BAY 11-7028 group and the PCV2 group. The results showed that PAMs infected with PCV2 induced IFN-I secretion through the cGAS/STING/TBK1/IRF3 signaling pathway.