The virulence factors and pathogenic mechanisms of Streptococcus pyogenes

AbstractStreptococcus pyogenes possesses a wide variety of virulence factors and can cause severe invasive infections. Most S. pyogenes express surface-located fibronectin-binding proteins as major invasion molecules. We identified 2 novel fibronectin-binding proteins (FbaA and FbaB) in S. pyogenes isolated from patients with severe invasive infection. Fba-deficient mutant strains showed significantly lower efficiency of invasion of human epithelial cells than that shown by an isogenic wild type strain. Furthermore, compared to mice infected with the isogenic wild-type strains, those infected with fba-deficient mutant strains showed decreased mortality. These findings suggest that Fba proteins are the causative agents for the development of severe invasive S. pyogenes infections.We know that few neutrophils migrate to S. pyogenes in severe streptococcal infection. We also found that complement C3b is degraded in the sera of patients with severe invasive S. pyogenes infections. Furthermore, it is now known that S. pyogenes SpeB is able to fragment neutrophil extracellular traps (NETs). SpeB appears to contribute to the escape of bacterial organisms from neutrophils by inactivating C3b and degrading NETs at the site of initial infection.Moreover, we have identified a C6-binding protein in cell-surface protein fractions from S. pyogenes. C6 is a component of the complement membrane attack complex (MAC). The C6-binding protein contributes to S. pyogenes evasion of the complement system by inhibiting MAC polymerization and bacteriolysis activity.We have confirmed that S. pyogenes is equipped with a wide variety of virulence factors to invade human tissue and escape from immunity