Mechanism research on staphylococcus aureus overload in hypertrophic scars mediates collagen production in scar fibroblasts through TLR-2/AP-1/TGF-β1 pathway
Objective:To investigate the mechanism underlying the influence of overloaded Staphylococcus aureus(S.aureus)on fibroblast collagen production in hypertrophic scars.Methods:The hypertrophic scar tissue and normal skin tissue of 16 inpatients with hypertrophic scar underwent scar resection and autologous skin transplantation were fixed sections.The bacteria in the tissues were observed by Gram staining,Staphylococcus aureus was detected by immunofluorescence,and the expression of toll-like receptor-2(TLR-2)and activator protein-1(AP-1)were detected by immunohistochemistry and western blot.Additionally,normal fibroblasts were cocultured with S.aureus at various concentrations,and the expression of TLR-2,AP-1,transforming growth factor β1(TGF-β1),and collagen typesⅠandⅢwere analyzed.Furthermore,the effects of blocking TLR-2 or AP-1 on TGF-β1 and collagen production were evaluated.Results:Gram staining revealed a significantly higher number of positive bacteria in hypertrophic scar tissues compared to normal skin,and immunofluorescence confirmed the presence of S.aureus.Both immunohistochemistry and western blot indicated that the expression of TLR-2 and AP-1 in scar was significantly higher than that in normal skin.1×105CFU/mL S.aureus can significantly promote the expression of TLR-2,AP-1,TGF-β1,and collagenⅠandⅡin normal fibroblasts.While the cells were treated with TLR-2 and AP-1 inhibitors respectively,it was found that TGF-β1 and collagen production were significantly inhibited.Conclusions:Staphylococcus aureus in hypertrophic scars is"overloaded"and promotes collagen production through TLR-2/AP-1/TGF-β1 pathway.Intervention of TLR-2 or AP-1 expression represents a promising therapeutic approach for scar management.
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