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Notch signaling contributes to the expression of inflammatory cytokines induced by highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) infection in porcine alveolar macrophages

文献类型： 外文期刊

作者： Lu, Yan 1 ; Zhang, Yanbing 1 ; Xiang, Xiao 1 ; Sharma, Mona 1 ; Liu, Ke 1 ; Wei, Jianchao 1 ; Shao, Donghua 1 ; Li, Beibe 1 ;

作者机构： 1.Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai, Peoples R China

2.Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Ann Arbor, MI USA

3.VA Ann Arbor Healthcare Syst, Ann Arbor, MI USA

关键词： HP-PRRSV; Notch signaling; Porcine alveolar macrophages; Inflammatory response

期刊名称：DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY （ 影响因子：3.636； 五年影响因子：3.654 ）

ISSN： 0145-305X

年卷期： 2020 年 108 卷

页码：

收录情况： SCI

摘要： Notch signaling, an evolutionarily conserved signal pathway has emerged as a key signal pathway to regulate host immune response but the contribution of Notch signaling to immune response in pigs remains unknown. Infection of porcine alveolar macrophages (PAM) with porcine reproductive and respiratory syndrome virus (PRRSV) triggers expression of Jagged1 mRNA, suggesting that Notch signaling might play a role in the immune response to PRRSV infection. To further explore it, we examined the expression profile of Notch molecules in PAM following a highly pathogenic PRRSV (HP-PRRSV) strain infection. We demonstrated that HP-PRRSV infection resulted in the induction of Notch ligands (Jagged1, Dll3, Dll4), the transcription factor RBP-J, and the target gene Hes1, consistent with activation of Notch signaling. Next, using DAPT treatment and the knockdown of RBP-J illustrated that inhibition of activation of Notch signaling attenuated induction of the inflammatory cytokines (TNF-alpha and IL-1 beta) instead of viral replication in PAM during HP-PRRSV infection. Furthermore, the knockdown of Jagged1, the most induced ligand not only inhibited activation of Notch signaling, but also reduced the expression of inflammatory cytokines without any influence in viral replication. Moreover, our data revealed that several signaling including NF-kappa B, MAPK and Notch signaling contributed to the induction of Jagged1 in PAM during HP-PRRSV infection. In summary, these findings reveal that Notch as an important signaling pathway could contribute to the regulation of inflammatory response induced by HP-PRRSV infection.

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