Regulation of type Ⅰ interferon secretion via the RIG-Ⅰ signaling pathway after PRV infection of mouse trigeminal ganglion cells
10.16303/j.cnki.1005-4545.2025.02.12
- VernacularTitle:PRV感染小鼠三叉神经节细胞后通过RIG-Ⅰ信号通路调控Ⅰ型干扰素分泌
- Author:
Zhengbo LIAO
1
;
Deyuan TANG
1
;
Zhiyong ZENG
1
;
Bin WANG
1
;
Tao HUANG
1
;
Xu CHEN
1
;
Shen-glin YUAN
1
;
Song HE
1
;
Piao ZHOU
1
;
Yinming MAO
1
Author Information
1. 贵州大学动物科学学院,贵州 贵阳 550025
- Publication Type:Journal Article
- Keywords:
PRV;
RIG-Ⅰ;
IRF3;
signaling pathway;
IFN-Ⅰ;
mice
- From:
Chinese Journal of Veterinary Science
2025;45(2):255-265
- CountryChina
- Language:Chinese
-
Abstract:
This study investigates the effects of pseudorabies virus(PRV)infection on the antiviral immune signaling pathways and type Ⅰ interferon factors in mouse trigeminal ganglion(TG)cells.In this experiment,primary TG cells were infected with PRV at a multiplicity of infection(MOI)of 1,while mice were infected via a drop-nose method using 106,29 TCID50 of PRV.Real-time fluorescence quantitative PCR(qPCR),Western blot and ELISA were used to assess gene tran-scription,protein expression,and the secretion of IFN-α and IFN-β.The results indicated that PRV infection of mouse TG primary cells led to alterations in the gene and protein expression of RIG-Ⅰ,MAVS,and IRF3,as well as the phosphorylation of IRF3 and IKBα both in vivo and ex vivo.ELISA results showed that PRV infection could regulate the secretion of IFN-α and IFN-β in mouse primary TG cells and mouse TGs.The results of RIG-Ⅰ signaling pathway-related proteins and the secretion of IFN-a and IFN-β were analyzed using Western blot after using siRNA to interfere with RIG-Ⅰ expression in TG cells.The results showed that siRIG-Ⅰ successfully inter-fered with RIG-Ⅰ protein expression in TG cells and caused changes in the expression of down-stream proteins such as MAVS and IRF3,and also regulated the secretion of IFN-α and IFN-β in TG cells.Furthermore,the results indicated that PRV infection induced the expression of RIG-Ⅰ in mouse TG progenitor cells,regulating the antiviral immune response of type Ⅰ interferon factors in TG cells through the RIG-Ⅰ-MAVS-IRF3 signaling axis.Notably,PRV inhibited the expression of IRF3 in TG cells while significantly upregulating the expression of IFN-β during the later stages of infection,which may be an important factor in the important reason for the rapid mortality ob-served in mice during the late stages of PRV infection.This experiment elucidates part of the anti-viral immune mechanism mediated by the RIG-Ⅰ-MAVS-IRF3 signaling pathway in regulating type Ⅰ interferon factor after PRV infection of mouse TG cells,as well as the discovery of differ-ent trends of IRF3 protein changes in vivo and ex vivo,laying the groundwork for future in-depth studies.
