Research Papers:

Swine IRF3/IRF7 attenuates inflammatory responses through TLR4 signaling pathway

Pei-Ge Chen, Yan-Jing Guan, Guang-Ming Zha, Xian-Qin Jiao, He-Shui Zhu, Cheng-Yu Zhang, Yue-Ying Wang and He-Ping Li _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:61958-61968. https://doi.org/10.18632/oncotarget.18740

Metrics: PDF 2027 views  |   HTML 3477 views  |   ?  


Pei-Ge Chen1,*, Yan-Jing Guan1,*, Guang-Ming Zha1,*, Xian-Qin Jiao1, He-Shui Zhu1, Cheng-Yu Zhang1, Yue-Ying Wang1 and He-Ping Li1

1Key Laboratory of Animal Biochemistry and Nutrition, Ministry of Agriculture, Henan Agricultural University, Zhengzhou, Henan, China

*These authors have contributed equally to this work

Correspondence to:

He-Ping Li, email: [email protected]

Yue-Ying Wang, email: [email protected]

Keywords: IRF3/IRF7, inflammatory response, overexpression, TLR4 signaling pathway, lipopolysaccharide

Received: April 27, 2017     Accepted: May 22, 2017     Published: June 28, 2017


To explore the role of IRF3/IRF7 during inflammatory responses, we investigated the effects of swine IRF3/IRF7 on TLR4 signaling pathway and inflammatory factors expression in porcine kidney epithelial PK15 cell lines. We successfully constructed eukaryotic vectors PB-IRF3 and PB-IRF7, transfected these vectors into PK15 cells and observed GFP under a fluorescence microscope. In addition, RT-PCR was also used to detect transfection efficiency. We found that IRF3/IRF7 was efficiently overexpressed in PK15 cells. Moreover, we evaluated the effects of IRF3/IRF7 on the TLR4 signaling pathway and inflammatory factors by RT-PCR. Transfected cells were treated with lipopolysaccharide (LPS) alone, or in combination with a TBK1 inhibitor (LiCl). We revealed that IRF3/IRF7 enhanced IFNα production, and decreased IL-6 mRNA expression. Blocking the TBK1 pathway, inhibited the changes in IFNα, but not IL-6 mRNA. This illustrated that IRF3/IRF7 enhanced IFNα production through TLR4/TBK1 signaling pathway and played an anti-inflammatory role, while IRF3/IRF7 decreased IL-6 expression independent of the TBK1 pathway. Trends in MyD88, TRAF6, TBK1 and NFκB mRNA variation were similar in all treatments. LPS increased MyD88, TRAF6, TBK1 and NFκB mRNA abundance in PBR3/PBR7 and PBv cells, while LiCl blocked the LPS-mediated effects. The levels of these four factors in PBR3/PBR7 cells were higher than those in PBv. These results demonstrated that IRF3/IRF7 regulated the inflammatory response through the TLR4 signaling pathway. Overexpression of swine IRF3/IRF7 in PK15 cells induced type I interferons production, and attenuated inflammatory responses through TLR4 signaling pathway.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 18740