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Review
. 2014 Feb 13;10(2):e1003871.
doi: 10.1371/journal.ppat.1003871. eCollection 2014 Feb.

Igniting the fire: Staphylococcus aureus virulence factors in the pathogenesis of sepsis

Michael E Powers  1 , Juliane Bubeck Wardenburg  2
Affiliations
Review

Igniting the fire: Staphylococcus aureus virulence factors in the pathogenesis of sepsis

Michael E Powers et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

I have read the journal's policy and have the following conflicts: JBW has the potential to receive royalties from Novartis Vaccines and Diagnostics in relation to patents owned by the University of Chicago. This does not alter our adherence to all PLOS policies on sharing data and materials.

Figures

Figure 1
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.
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