LPS induces activation of the TLR4 pathway in fibroblasts and promotes skin scar formation through collagen I and TGF-β in skin lesions.

Hypertrophic scars are proliferative diseases of dermal fibroblasts that produce abundant amounts of collagen and extracellular matrix in the skin after severe burns, inflammation and trauma. Hypertrophic scars affect the daily life of patients and cause a series of problems. The biological mechanism of hypertrophic scar formation is still unclear and has received much attention in plastic surgery. Therefore, we hypothesized that LPS can activate TLR4 signaling, leading to the overexpression of collagen I and TGF-β and the induction of hypertrophic scar formation. In the present study, we used LPS to validate the role of the TLR4 signaling pathway in 3T3-L1 cells and hypertrophic scar mouse models to determine the role of the TLR4 signaling pathway in proliferative scar formation . The results suggested that LPS leads to the activation of the TLR4 pathway in fibroblasts, and inhibitor experiments confirmed that TLR4 is involved in the expression of collagen I by regulating the NF-κB pathway. The mouse skin wound model experiments demonstrated that TLR4 is involved in wound healing and scar formation. Our experiments demonstrated that the TLR4-IRAK4-NF-κB pathway is involved in the production of hypertrophic scars and wound healing.