Pierre Fabre Dermo-Cosmétique and Personal Care, Toulouse, France.
Direction Médicale DUCRAY, Lavaur, France.
J Eur Acad Dermatol Venereol. 2023 Mar;37 Suppl 2:3-11. doi: 10.1111/jdv.18794.
Acne vulgaris is a common chronic inflammatory skin disease of the pilosebaceous units. Four factors contribute to acne: hyperseborrhea and dysseborrhea, follicular hyperkeratinisation, skin microbiome dysbiosis and local immuno-inflammation. Recent key studies have highlighted a better understanding of the important role of Cutibacterium acnes (C. acnes) in the development of acne. Three major findings in the last decade include: (1) the ability of C. acnes to self-organize in a biofilm associated with a more virulent activity, (2) the loss of the C. acnes phylotype diversity and (3) the central role of the Th17 pathway in acne inflammation. Indeed, there is a close link between C. acnes and the activation of the Th17 immuno-inflammatory pathway at the initiation of acne development. These mechanisms are directly linked to the loss of C. acnes phylotype diversity during acne, with a predominance of the pro-pathogenic phylotype IA1. This specifically contributes to the induction of the Th17-mediated immuno-inflammatory response involving skin cells, such as keratinocytes, monocytes and sebocytes. These advancements have led to new insights into the underlying mechanisms which can be harnessed to develop novel treatments and diagnostic biomarkers. A major disadvantage of traditional treatment with topical antibiotics is that they induce cutaneous dysbiosis and antimicrobial resistance. Thus, future treatments would no longer aim to 'kill' C. acnes, but to maintain the skin microbiota balance allowing for tissue homeostasis, specifically, the restoration of C. acnes phylotype diversity. Here, we provide an overview of some of the key processes involved in the pathogenesis of acne, with a focus on the prominent role of C. acnes and the Th17-inflammatory pathways involved.
寻常痤疮是一种常见的毛囊皮脂腺单位慢性炎症性皮肤病。有四个因素促成痤疮的发生：皮脂过度分泌和皮脂溢出、滤泡过度角化、皮肤微生物组失调和局部免疫炎症。最近的关键研究强调了更好地理解痤疮发病过程中痤疮丙酸杆菌（C. acnes）的重要作用。过去十年中的三项主要发现包括：（1）C. acnes 能够在生物膜中自我组织，从而具有更强的致病性，（2）C. acnes 菌株多样性的丧失，以及（3）Th17 途径在痤疮炎症中的核心作用。实际上，C. acnes 与痤疮发病过程中 Th17 免疫炎症途径的激活之间存在密切联系。这些机制与痤疮过程中 C. acnes 菌株多样性的丧失直接相关，其中优势的致病性菌株是 IA1。这特别有助于诱导涉及皮肤细胞（如角质形成细胞、单核细胞和皮脂腺）的 Th17 介导的免疫炎症反应。这些进展为潜在机制提供了新的见解，可用于开发新的治疗方法和诊断生物标志物。传统局部用抗生素治疗的一个主要缺点是，它们会导致皮肤微生物组失调和抗微生物药物耐药性。因此，未来的治疗方法将不再旨在“杀死”C. acnes，而是维持皮肤微生物组平衡，以允许组织内稳态，特别是恢复 C. acnes 菌株多样性。在这里，我们概述了痤疮发病机制中涉及的一些关键过程，重点介绍了 C. acnes 的突出作用和涉及的 Th17 炎症途径。
