• Zhigang Xu, Chuantao Cheng, Yangang Zhang, Danyang Yang, Wenwen Jing, Xin Liu, and Xiaoli Li.
• Department of Dermatology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi Wu Road, No 157, Xi'an 710004, China; Department of Burns and Cutaneous Surgery, Xijing Hospital, Air Force Medical University, West Chang-le Road, No 127, Xi'an 710032, China.
• Burns. 2023 Dec 1; 49 (8): 199720061997-2006.

AbstractSkin scarring is a frequent complication of the wound healing process. Bacterial contamination and prolonged inflammation in wounds are thought to play significant roles during scar formation, but little is known about their specific mechanisms of action. In this study, hypertrophic scar derived fibroblasts (HSFs) and paired normal skin derived fibroblasts (NSFs) were used to evaluate the effects of lipopolysaccharide (LPS) on inflammation-induced skin scarring and explore the inflammation-mediated mechanism of activity of LPS on dermal fibroblasts. LPS was found to significantly upregulate the expression of the proinflammatory molecules TLR4, Myd88, TRAF6, and p65, and the fibrosis-related proteins Col I, Col III, and α-SMA, in NSFs. Blocking Myd88 expression with T6167923 downregulated the expression of Col I, Col III, and α-SMA, whereas activating Myd88 expression with CL075 significantly upregulated their expression in LPS-treated NSFs. LPS was found to delay wound healing and increase skin scarring in cell and mouse models. These results showed that LPS could induce scar formation through the TLR4/Myd88 signaling pathway in dermal fibroblasts, suggesting that the downregulation of excessive inflammation in wound tissues inhibits skin scarring and improves scar appearance.Copyright © 2023 Elsevier Ltd and International Society of Burns Injuries. All rights reserved.

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