Figure 1.

Therapeutic targeting of NETs improves primary intention wound healing. In all animals a 2.5 cm long laparotomy was performed. For the wildtype and knockout mice two timepoints (72 h, 21 days) were performed. Controls n=6, DNase1 n=6, DNase1-KO n=5, Pad4-KO n=6. (A, B) Animals that received DNase1 had significantly superior scar scores than controls. In mice that were unable to produce NETs (Pad4-KO) a similar effect was found. (C–E) Animals with DNase1 treatment or animals without NETs showed a significantly faster switch from collagen 3 to 1 and better collagen alignment indicating a faster maturation of the scar. (F) As previously reported DNase1 reduced Fibrin levels in the scar. (G) SMA was not affected by DNase1 treatment or in animals without NETs. Data shown as Mean ± SD. Comparison was performed always in comparison with controls. Statistics: mixed-effect model with Geisser-Greenhouse correction as well as Dunnett’s multiple comparison test. *DNase1 vs. controls. ^#PAD4-KO vs. controls.