Fig. 4

Agr system in systemic infection. A In the bloodstream infection, S. aureus PSMα can lyse neutrophils after phagocytosis, resulting in re-entry of the pathogen into the bloodstream. Additionally, S. aureus α-toxin can lead to endothelial damage, platelet aggregation, and overt inflammatory responses, resulting in life-threatening disseminated intravascular coagulation (DIC). In mice S. aureus sepsis experiments, bacteria are trapped in Kupffer cells, but survive and multiply within cells, escape to the peritoneum and become trapped in peritoneal macrophage, and eventually disseminate to other organs. α-toxin is involved in the liver damage and intracellular survival in this pathogenesis. B Agr defective S. aureus reportedly produces dense biofilm and escapes from immune attack by not eliciting strong inflammatory response. C S. aureus population is not always homogeneous in Agr activity but can produce an agr mutant or revertant within them to coordinately survive in various conditions in hospitals. PSM phenol-soluble modulin