Fig 1.
Mechanisms of Staphylococcus aureus SspA-mediated virulence in the skin.
S. aureus SspA serves several identified functions during skin infection, including disruption of the epidermal barrier in the upper epidermis, potentially through tight junction protein degradation (A); degradation of immune factors in the lower epidermis/upper dermis (B); modification of its own secreted and surface-associated virulence factors (C); and induction of itch via PAR1 activation in the lower epidermis (D). The SspA C-terminal domain (CTD) may contribute to virulence, possibly by mediating protein-protein interactions with skin components (E). FnBPs, fibronectin-binding proteins; Atl, autolysin; IgG, immunoglobulin G; AMPs, antimicrobial peptides; PAR1, protease-activated receptor 1; CTD, C-terminal domain; PPII, type II polyproline helix. Created with BioRender.