The C-Terminal Repeat Units of SpaA Mediate Adhesion of <i>Erysipelothrix rhusiopathiae</i> to Host Cells and Regulate Its Virulence
Chao Wu,
Zhewen Zhang,
Chao Kang,
Qiang Zhang,
Weifeng Zhu,
Yadong Zhang,
Hao Zhang,
Jingfa Xiao,
Meilin Jin
Affiliations
Chao Wu
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China
Zhewen Zhang
National Genomics Data Center, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China
Chao Kang
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China
Qiang Zhang
College of Biomedicine and Health, Huazhong Agricultural University, Wuhan 430070, China
Weifeng Zhu
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China
Yadong Zhang
National Genomics Data Center, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China
Hao Zhang
National Genomics Data Center, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China
Jingfa Xiao
National Genomics Data Center, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China
Meilin Jin
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China
Erysipelothrix rhusiopathiae is a causative agent of erysipelas in animals and erysipeloid in humans. However, current information regarding E. rhusiopathiae pathogenesis remains limited. Previously, we identified two E. rhusiopathiae strains, SE38 and G4T10, which were virulent and avirulent in pigs, respectively. Here, to further study the pathogenic mechanism of E. rhusiopathiae, we sequenced and assembled the genomes of strains SE38 and G4T10, and performed a comparative genomic analysis to identify differences or mutations in virulence-associated genes. Next, we comparatively analyzed 25 E. rhusiopathiae virulence-associated genes in SE38 and G4T10. Compared with that of SE38, the spaA gene of the G4T10 strain lacked 120 bp, encoding repeat units at the C-terminal of SpaA. To examine whether these deletions or splits influence E. rhusiopathiae virulence, these 120 bp were successfully deleted from the spaA gene in strain SE38 by homologous recombination. The mutant strain ΔspaA displayed attenuated virulence in mice and decreased adhesion to porcine iliac artery endothelial cells, which was also observed using the corresponding mutant protein SpaA’. Our results demonstrate that SpaA-mediated adhesion between E. rhusiopathiae and host cells is dependent on its C-terminal repeat units.
