Figure 1.
Overview of S. aureus virulence factors that contribute to the pathogenesis of sepsis.
(a) Leukocytes are targeted and injured by bi-component leukocidins (PVL, LukAB/GH, LukED, and Hlg, blue and orange), phenol-soluble modulins (PSM, purple), and α-toxin (Hla, green). (b) Inhibition of host complement pathways occurs through Chemotaxis Inhibitory Protein of Staphylococci (CHIPS) binding to the C5a receptor and (c) Staphylococcal Complement Inhibitor (SCIN)-mediated blockade of C3 convertase activity. (d) Staphylococcal protein A (SpA) binds to host antibodies, preventing opsonophagocytosis and contributing to apoptotic death of B cells. (e) Coagulase (Coa) and von Willebrand factor binding protein (vWbp) initiate fibrin clot formation, facilitating the formation of staphylococcal aggregates in the blood through the action of clumping factors A and B (ClfA/B). (f) Platelet traps surround staphylococci that adhere to macrophage-like Kupffer cells in the liver sinusoid. (g) Fibronectin-binding proteins A and B (FnBPA/B) bind to integrin α5β1, enabling the tethering of S. aureus to endothelial cells in the context of blood flow. (h) Expression of S. aureus α-toxin (Hla) causes direct injury to the endothelium, disrupting the integrity of the endothelial barrier.