Abstract

This study was conducted to reveal the process of atrophic acne scar formation in histological and molecular views. Thirty subjects with acne were divided into two groups; fifteen were prone to acne scar (APS) and the others were not prone to acne scar (ANS). Skin samples of acne lesions were obtained on day 1, 3 and 7 after their onset. Elastic fibers, collagen 1 and collagen 3 were significantly decreased and their recovery was delayed in APS compared to those in ANS. On the other hand, the production of neutrophil elastase, matrix metalloproteinases (MMP)-1, MMP-2 and MMP-3 was substantially increased in APS compared to that in ANS. More severe inflammation with elevated various proinflammatory cytokines including IL-1α, IL-1β, IL-6 and TNF-α was observed in APS than in ANS, implicating that excessive inflammation contributes to the aberrant ECM degradation and healing. In this process, it was found that increased TGF-β1 in APS may play a crucial role in aggravating inflammation via activating phospho-TAK1 and NF-κB p65. These results propose the detailed pathogenesis of atrophic acne scarring and ultimately provide a basis of a new therapeutic approach in atrophic acne scar.

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