Staphylococcus aureus gamma-hemolysin CB (HlgCB)

Staphylococcus aureus gamma-hemolysin CB (HlgCB) is a bicomponent pore-forming toxin composed of HlgC (S-class component) and HlgB (F-class component), encoded by the hlgCB genes in nearly all human S. aureus isolates. It assembles into hetero-oligomeric beta-barrel pores (e.g., octameric or 3C3B/4C4B structures) on host cell membranes, leading to hemolysis, leukotoxicity, and cytotoxicity primarily against phagocytic cells like neutrophils and macrophages via receptors such as C5aR and C5L2.[2][3][4][5][7] HlgCB expression is regulated by factors like agr, SarA, and SaeRS systems, with variations due to SNPs in promoter and 5' UTR regions affecting translation and levels among clinical strains.[6] In disease, HlgCB contributes to S. aureus virulence in infections including pneumonia, bacteremia, endocarditis, and peritonitis by lysing immune cells, evading phagocytosis, and promoting inflammation through inflammasome activation and cytokine release like IL-1β.[4][5][6] Its high prevalence and consistent expression distinguish it as a major secreted leukocidin compared to less common toxins like PVL.[5] No approved drugs directly target HlgCB, reflecting its role as a bacterial virulence factor rather than a host therapeutic target.[1][3][4][5][6][10]

Other names

gamma-hemolysin CBHlgC/HlgBHlgCB toxin