Received: March 25, 2016; Revised: September 30, 2016; Accepted: November 23, 2016; Published online: January 4, 2017.
Streptococcus suis is regarded as one of the major pathogens of pigs while S. suis type 2 (SS2) is considered to be a zoonotic bacterium for its ability to cause meningitis and streptococcal toxic shock-like syndrome in humans. Many bacterial species contain genes encoding serine/threonine protein phosphatases (STP) responsible for dephosphorylation of their substrates in a single reaction step. This study was aimed to investigate the role of stp1 in pathogenesis of SS2. An isogenic stp1 mutant (Δstp1) was constructed from the SS2 strain ZJ081101. The Δstp1 mutant exhibited significant increase in adhesion to HEp-2 and bEnd.3 cells as well as in survival within RAW264.7 cells, as compared to its parent strain. Increased survival in macrophage cells might be related to resistance to reactive oxygen species since the stp1 mutant was more resistant to paraquat-induced oxidative stress than its parent strain. However, deletion of stp1 significantly attenuated virulence of SS2 in mice, as shown by nearly twice the LD50 value in the murine model and lower bacterial load in organs and blood of mice than its parent strain. We conclude that Stp1 plays an essential role in SS2 virulence.
Keywords: Streptococcus suis type 2, serine/threonine protein phosphatase, virulence