Abstract
Streptococcus suis is an emerging zoonotic pathogen causing streptococcal toxic shock like syndrome (STSLS), meningitis, septicemia, and even sudden death in human and pigs. Serious septicemia indicates this bacterium can evade the host complement surveillance. In our previous study, a functionally unknown protein SntA of S. suis has been identified as a heme-binding protein, and contributes to virulence in pigs. SntA can interact with the host antioxidant protein AOP2 and consequently inhibit its antioxidant activity. In the present study, SntA is identified as a cell wall anchored protein that functions as an important player in S. suis complement evasion. The C3 deposition and membrane attack complex (MAC) formation on the surface of sntA-deleted mutant strain ΔsntA are demonstrated to be significantly higher than the parental strain SC-19 and the complementary strain CΔsntA. The abilities of anti-phagocytosis, survival in blood, and in vivo colonization of ΔsntA are obviously reduced. SntA can interact with C1q and inhibit hemolytic activity via the classical pathway. Complement activation assays reveal that SntA can also directly activate classical and lectin pathways, resulting in complement consumption. These two complement evasion strategies may be crucial for the pathogenesis of this zoonotic pathogen. Concerning that SntA is a bifunctional 2′,3′-cyclic nucleotide 2′-phosphodiesterase/3′-nucleotidase in many species of Gram-positive bacteria, these complement evasion strategies may have common biological significance.
Highlights
Streptococcus suis are recognized as an important swine and human pathogen [1]
The growth curves of S. suis presented by OD and colony forming unit (CFU) were measured before infection in mice
We found that the surface heme-binding protein SntA of S. suis [24] contributes to the resistance of C3 deposition and membrane attack complex (MAC) formation on bacterial surface, the abilities of anti-phagocytosis, survival in blood, and in vivo colonization
Summary
Streptococcus suis are recognized as an important swine and human pathogen [1]. Two large-scale outbreaks of severe human SS2 infection occur in 1998 and 2005 in China causing 229 infections and 52 deaths [3, 4]. An early burst of inflammatory cytokines could result in the STSLS with death as quickly as 13 h after SS2 infection, and subsequently SS2 breaks through blood–brain barrier (BBB) to cause disease, meningitis [1, 5]. Bacterial pathogens evade host innate immune defenses and maintain a high dose in blood causing bacteremia and septicemia. During these processes, the host complement system is an important factor facilita ting clearance of bacterial pathogens [6, 7]
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