2. Academic Validation
  3. Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) induces IL-6 production through TAK-1/JNK/AP-1 and TAK-1/NF-κB signaling pathways

Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) induces IL-6 production through TAK-1/JNK/AP-1 and TAK-1/NF-κB signaling pathways

  • Vet Microbiol. 2021 May:256:109061. doi: 10.1016/j.vetmic.2021.109061.
Yangyang Xu 1,  Honglei Wang 1,  Xuan Zhang 1,  Xiaojie Zheng 1,  Yingqi Zhu 1,  Haige Han 1,  Wen-Hai Feng 2
Affiliations

Affiliations

  • 1 State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Ministry of Agriculture Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Department of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China.
  • 2 State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Ministry of Agriculture Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China; Department of Microbiology and Immunology, College of Biological Sciences, China Agricultural University, Beijing, 100193, China. Electronic address: [email protected].
PMID: 33836390 DOI: 10.1016/j.vetmic.2021.109061
Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) mainly infects monocyte/macrophage lineage and regulates the production of cytokines to influence host immune responses. Interleukin-6 (IL-6) is originally identified as a B-cell stimulatory factor and has important functions in regulating immune response, hemopoiesis, and inflammation. In this study, we verified that highly pathogenic PRRSV (HP-PRRSV) Infection up-regulated IL-6 production in vivo and in vitro. Subsequently, we demonstrated that HP-PRRSV Infection activated JNK and NF-κB signaling pathways to enhance IL-6 expression. We further showed that TAK-1 was important in the activation of JNK and NF-κB pathways following HP-PRRSV Infection. Moreover, AP-1 and NF-κB binding motifs were found in the cloned porcine IL-6 (pIL-6) promoter, and deletion of these motifs abrogated the activation of pIL-6 promoter by HP-PRRSV, suggesting that IL-6 expression is dependent on AP-1 and NF-κB activation. These findings imply that IL-6 induced by HP-PRRSV Infection is dependent on the activation of TAK-1/JNK/AP-1 and TAK-1/NF-κB signaling pathways.

Keywords

AP-1; Highly pathogenic PRRSV; IL-6; JNK; NF-κB; TAK-1.

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