A phase 1 randomized controlled trial of a peptide-based group A streptococcal vaccine in healthy volunteers.

Background: Group A streptococci (Strep A) orStreptococcus pyogenes is a major human pathogen causing an estimated 500,000 deaths worldwide each year. Disease can range from mild pharyngitis to more severe infections, such as necrotizing fasciitis, septicemia, and toxic shock syndrome. Untreated, Strep A infection can lead to the serious post streptococcal pathologies of rheumatic fever/rheumatic heart disease and post-streptococcal glomerulonephritis.

Disruption of IL-17-mediated immunosurveillance in the respiratory mucosa results in invasive infection.

Introduction: is a Gram-positive pathogen that causes a significant global burden of skin pyoderma and pharyngitis. In some cases, infection can lead to severe invasive streptococcal diseases. Previous studies have shown that IL-17 deficiency in mice (IL-17) can reduce clearance from the mucosal surfaces.

Polymeric epitope-based vaccine induces protective immunity against group A Streptococcus.

Group A Streptococcus (Strep A) is a life-threatening human pathogen with no licensed vaccine. Here, we used a biopolymer particle (BP) approach to display repeats of Strep A vaccine candidate peptides p*17 and K4S2 derived from M and non-M protein, respectively. BPs densely displaying both peptides (BP-p*17-S2) were successfully assembled in one-step inside an engineered endotoxin-free Escherichia coli strain.

Streptolysin O Deficiency in Streptococcus pyogenes M1T1 Mutant Strain Attenuates Virulence in and Infection Models.

Mutation within the Streptococcus pyogenes ( group A; Strep A) regulatory system has been associated with a hypervirulent phenotype resulting from the upregulation of several virulence factors, including the pore-forming toxin, streptolysin O (SLO). In this study, we utilized a range of mutants, including M1T1 clonal strains (5448 and a mutant generated through mouse passage designated 5448AP), to investigate the contribution of SLO to the pathogenesis of mutant Strep A disease. Up-regulation of in 5448AP resulted in increased SLO-mediated hemolysis, decreased dendritic cell (DC) viability post coculture with Strep A, and increased production of tumor necrosis factor (TNF) and monocyte chemoattractant protein 1 (MCP-1) by DCs.