EspP2 Regulates the Adhesion of Glaesserella parasuis via Rap1 Signaling Pathway

Author:

Tang Xinwei1,Xu Shiyu1,Yang Zhen1,Wang Kang1,Dai Ke1,Zhang Yiwen1,Hu Bangdi1,Wang Yu1,Cao Sanjie1ORCID,Huang Xiaobo1,Yan Qigui1,Wu Rui1ORCID,Zhao Qin1ORCID,Du Senyan1ORCID,Wen Xintian1,Wen Yiping1

Affiliation:

1. Research Center of Swine Disease, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China

Abstract

Different levels of EspP2 expression are seen in strains of Glaesserella parasuis with high and low pathogenicity. As a potential virulence factor for G. parasuis, the pathogenic mechanism of EspP2 in infection of host cells is not clear. To begin to elucidate the effect of EspP2 on virulence, we used G. parasuis SC1401 in its wild-type form and SC1401, which was made EspP2-deficient. We demonstrated that EspP2 causes up-regulation of claudin-1 and occludin expression, thereby promoting the adhesion of G. parasuis to host cells; EspP2-deficiency resulted in significantly reduced adhesion of G. parasuis to cells. Transcriptome sequencing analysis of EspP2-treated PK15 cells revealed that the Rap1 signaling pathway is stimulated by EspP2. Blocking this pathway diminished occludin expression and adhesion. These results indicated that EspP2 regulates the adhesion of Glaesserella parasuis via Rap1 signaling pathway.

Funder

the Key R&D support plan of Chengdu Science and Technology Bureau

Publisher

MDPI AG

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