Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Acne, Rosacea, Seborrheic Dermatitis and Hidradenitis Suppurativa Research Laboratory, Seoul National University Hospital, Seoul, Republic of Korea.
Br J Dermatol. 2019 Dec;181(6):1226-1237. doi: 10.1111/bjd.17851. Epub 2019 Jul 9.
Atrophic acne scar, a persistent sequela from acne, is undesirably troubling to many patients due to its cosmetic and psychosocial aspects. Although there have been some reports emphasizing the role of early inflammatory responses in atrophic acne scarring, evolving perspectives on the detailed pathogenic processes are promptly needed.
Examining the histological, immunological and molecular changes in early acne lesions susceptible to atrophic scarring can provide new insights to understand the pathophysiology of atrophic acne scar.
We experimentally validated several early fundamental hallmarks accounting for the transition of early acne lesions to atrophic scars by comparing molecular profiles of skin and acne lesions between patients who were prone to scar (APS) or not (ANS).
In APS, compared with ANS, devastating degradation of elastic fibres and collagen fibres occurred in the dermis, followed by their incomplete recovery. Abnormally excessive inflammation mediated by innate immunity with T helper 17 and T helper 1 cells was observed. Epidermal proliferation was significantly diminished. Transforming growth factor (TGF)-β1 was drastically elevated in APS, suggesting that aberrant TGF-β1 signalling is an underlying modulator of all of these pathological processes.
These results may provide a basis for understanding the pathogenesis of atrophic acne scarring. Reduction of excessive inflammation and TGF-β1 signalling in early acne lesions is expected to facilitate the protection of normal extracellular matrix metabolism and ultimately the prevention of atrophic scar formation. What's already known about this topic? The dermis of atrophic acne scars shows alteration of extracellular matrix components such as collagen fibres. Inflammation in acne lesions is associated with the development of acne scars. What does this study add? Abnormalities in the metabolism of collagen fibres and elastic fibres were observed in the early developmental stages of acne lesions that were progressing into atrophic scars. Exacerbated inflammation and aberrant epidermal proliferation by increased transforming growth factor (TGF)-β1 signalling may affect the abnormal extracellular matrix metabolism. What is the translational message? Abnormal changes in elastic fibres and collagen fibres are found in the early developmental process of acne in patients who are prone to atrophic scarring. An early treatment regimen strongly inhibiting inflammation and TGF-β1 signalling to help the normal recovery of the extracellular matrix components is required to prevent atrophic scarring.
萎缩性痤疮瘢痕是痤疮的一种持续性后遗症，由于其美观和心理社会方面的原因，给许多患者带来了困扰。尽管已有一些报告强调了早期炎症反应在萎缩性痤疮瘢痕形成中的作用，但仍需要及时了解详细的发病机制。
研究早期易发生萎缩性瘢痕的痤疮皮损的组织学、免疫学和分子变化，可为了解萎缩性痤疮瘢痕的病理生理学提供新的认识。
我们通过比较易发生瘢痕（APS）和不易发生瘢痕（ANS）患者的皮肤和痤疮皮损的分子谱，实验验证了几种早期基本特征，这些特征解释了早期痤疮皮损向萎缩性瘢痕的转变。
与 ANS 相比，APS 患者的真皮中弹性纤维和胶原纤维严重降解，随后无法完全恢复。观察到固有免疫介导的异常过度炎症，伴有辅助性 T 细胞 17 和 T 辅助 1 细胞。表皮增殖明显减少。转化生长因子（TGF）-β1 在 APS 中明显升高，表明异常 TGF-β1 信号是所有这些病理过程的潜在调节剂。
这些结果可能为理解萎缩性痤疮瘢痕形成的发病机制提供依据。减少早期痤疮皮损中的过度炎症和 TGF-β1 信号有望促进正常细胞外基质代谢的保护，最终预防萎缩性瘢痕形成。
已知该主题的内容是什么？萎缩性痤疮瘢痕的真皮中存在细胞外基质成分（如胶原纤维）的改变。痤疮皮损中的炎症与痤疮瘢痕的发展有关。
本研究增加了什么？在进展为萎缩性瘢痕的痤疮皮损的早期发育阶段观察到胶原纤维和弹性纤维代谢异常。增加的转化生长因子（TGF）-β1 信号的炎症加剧和表皮增殖异常可能影响异常细胞外基质代谢。
这有什么转化意义？在易发生萎缩性瘢痕的患者的痤疮早期发育过程中发现弹性纤维和胶原纤维的异常变化。需要采用强烈抑制炎症和 TGF-β1 信号的早期治疗方案，帮助细胞外基质成分的正常恢复，以预防萎缩性瘢痕形成。
