Fig. 4.

Nonlytic NET formation promoted by S. aureus and S. aureus virulence factors. S. aureus cells activate complement receptor or TLR2 on neutrophils. Afterwards, PAD4 is activated and along with elastase translocates to the nucleus where they induce chromatin decondensation. Chromatin decorated with cytosolic proteins is expelled via vesicles without plasma membrane disruption. Loss of the nucleus does not compromise processes such as phagocytosis, chemotaxis and release of cytotoxic molecules. Paradoxically, S. aureus virulence factors such as nuclease, Eap, and FnBPB can interact with specific components of NETs and block their anti-bacterial activity.