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Study Design/Patients and Methods
A 19-year-old male was reported to have a postoperative facial trauma suture as a result of being involved in a car accident. Red light-emitting diode (LED) therapy (20 min, 96 J/cm², 633 nm), Botulinum Toxin Type A 36 IU injection, BroadBand Light and Er:YAG laser at various stages of wound healing were applied as...
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keloids and hypertrophic scars are cosmetic problems with significant morbidity. Many clinical modalities were tried in order to modulate the disfigurement related to these pathologic scars. to evaluate the clinical and histopathological effects of Botulinum toxin type A (BTX‐A) injection on keloids and hypertrophic scars. 12 patients with keloids...
Citations
... Scar formation is the final stage of wound healing, which involves the degeneration of neovascularization and concomitant reconstruction of the extracellular matrix (ECM), resulting in the development of organized collagen fibrils that serve as the basis of normal scarring [33]. When these processes are disturbed, pathological healing results in an ulcerative chronic wound, a hypertrophic scar or a keloid [34]. ...
Background
Inflammation is an important factor in pathological scarring. The role of neutrophils, one of the most important inflammatory cells, in scar hyperplasia remains unclear. The purpose of this article is to study the correlation between neutrophil extracellular traps (NETs) and scar hyperplasia and identify a new target for inhibiting scar hyperplasia.
Methods
Neutrophils were isolated from human peripheral blood by magnetic-bead sorting. NETs in plasma and scars were detected by enzyme-linked immunosorbent assays (ELISAs), immunofluorescence and flow cytometry. Immunohistochemistry was used to assess neutrophil (CD66B) infiltration in hypertrophic scars. To observe the entry of NETs into fibroblasts we used immunofluorescence and flow cytometry.
Results
We found that peripheral blood neutrophils in patients with hypertrophic scars were more likely to form NETs (p < 0.05). Hypertrophic scars showed greater infiltration with neutrophils and NETs (p < 0.05). NETs activate fibroblasts in vitro to promote their differentiation and migration. Inhibition of NETs with cytochalasin in wounds reduced the hyperplasia of scars in mice. We induced neutrophils to generate NETs with different stimuli in vitro and detected the proteins carried by NETs. We did not find an increase in the expression of common scarring factors [interleukin (IL)-17 and transforming growth factor-β (TGF-β), p > 0.05]. However, inhibiting the production of NETs or degrading DNA reduced the differentiation of fibroblasts into myofibroblasts. In vitro, NETs were found to be mediated by Toll-like receptor 9 (TLR-9) in fibroblasts and further phosphorylated nuclear factor Kappa-B (NF-κB). We found that IL-6, which is downstream of NF-κB, was increased in fibroblasts. Additionally, IL-6 uses autocrine and paracrine signaling to promote differentiation and secretion.
Conclusions
Our experiments found that NETs activate fibroblasts through the TLR-9/NF-κB/IL-6 pathway, thereby providing a new target for regulating hypertrophic scars.
