Contribution of the srtBCD pilus cluster genes sbp1 and sbp3 to the virulence of Streptococcus suis serotype 2 sequence type 1

Streptococcus suis is an important zoonotic bacterial pathogen that causes substantial economic losses to the porcine industry and serious invasive infection in humans. Many virulence factors have been characterized as being involved in S. suis virulence and pathogenesis. Among these, the srtBCD pilus cluster gene, which encodes three type C sortases ( srtB, srtC , and srtD ) and four pilin subunit proteins, sbp1-sbp4 , is associated with disease-causing S. suis isolates. In this study, we constructed mutant strains devoid of sbp1 and sbp3 in a virulent S. suis serotype 2 sequence type 1 strain, and evaluated the impact on virulence using both in vitro and in vivo models of infection. This study identifies sbp1 and sbp3 contribute to host–pathogen interactions. Inactivation of either gene reduced the bacterium’s ability to damage epithelial cells, attach to host cells, and invade them, demonstrating their role in the early stages of infection. In addition, inactivation of sbp1 or sbp3 decreased the expression of the sortase-associated gene cluster ( SSU1889, SSU1886, srtB, srtC, srtD ) and several virulence-related genes, including the adhesin gene ssfsb , eno and the cytolysin gene sly , suggesting that these proteins influence a broader network. Among the two proteins, sbp1 appeared to have a greater impact on virulence, as the Δsbp1 mutant showed stronger reductions in virulence gene expression and caused lower mortality in mice, although statistical does not significant, suggesting that sbp1 plays a more prominent role than sbp3 in pathogenicity.