Figure 4 NETs are essential for limiting acute S.

aureus dissemination

Bacterial Dissemination
Skin of mice pretreated with either DNase or saline Intraperitoneal Injection of live luminescent S. aureus Minimally invasive nonsurgical luminiscent photon imaging within the mouse skin Currently, no specific inhibitor of NETosis exists, so exogenous DNase treatment was used to break down NETs. Follow staphylococcus skin infections over time: S. aureus quantified within the skin at 1 h, 4 h and 8 h after infection. Mice treated with or without DNase had comparable S. aureus levels of luminescent photons within the skin at 1 h, but DNase treatment decreased luminescence within 4 h. This shows that S.aureus has disseminated from skin to other parts in the presence of DNase.

Figure 4

Bacterial Dissemination
DNase did not alter bacterial growth in culture (data not shown). Bacteremia = Bacterial dissemination from the skin to the blood Disruption of NETs resulted in a significant increase in bacteremia at 4 h NET-disruption resulted in a decrease of skin CFUs at 24 h This indicates that bacteria can rapidly escape the portal of entry in the absence of NET trapping.

Figure 4

Supplementary Figure 4c: dissemination in mutant mice that lack NETosis

Determination of blood CFUs at 5 h. C3/ mice, which were deficient in both phagocytosis and NETosis, had more severe bacteremia than did Tlr2/ mice, which could phagocytose but not NETose.