痤疮中微生物范式的演变

摘要(中文译文)

本综述探讨寻常痤疮的微生物学。寻常痤疮是一种毛囊皮脂腺单位的慢性炎症性疾病，影响大多数青少年，并可持续至成年期。当前的标准治疗主要采用抗菌干预措施，这是基于将痤疮丙酸杆菌视为病原体的传统观点。替代治疗方案则由“粉刺开关”假说提出，该假说将痤疮归因于LRIG1+皮脂祖细胞的异常分化。尽管有强有力的证据支持这一观点，但它无法解释抗菌干预措施的有效性。我们提出一种统一机制，即痤疮丙酸杆菌系统发育型IA1可作为粉刺开关的触发因素。与共生菌株不同，系统发育型IA1具有高脂肪酶活性，可将皮脂甘油三酯水解为游离脂肪酸，特别是棕榈酸。该代谢产物刺激LRIG1+祖细胞，诱导炎症和初始粉刺形成。本综述讨论了痤疮丙酸杆菌的系统发育型，重点介绍了IA1已知的毒力因子，如增强的生物膜形成能力。我们评估了新旧抗菌药物的疗效和局限性，并指出能够选择性清除痤疮丙酸杆菌IA1的新型材料可减少非炎症性痤疮皮损，从而支持该系统发育型在痤疮发病机制中的关键作用。

Abstract

This review discusses the microbiology of acne vulgaris, a chronic inflammatory condition of the pilosebaceous unit that affects most adolescents and can persist into adulthood. The current standard of care consists largely of antibacterial interventions, based on the traditional view of as a pathogen. Alternative treatments are suggested by the "comedo switch" hypothesis, which attributes acne to aberrant differentiation of LRIG1+ sebaceous progenitor cells. While there is strong evidence to support this idea, it does not explain the efficacy of antibacterial interventions. We propose a unified mechanism wherein phylotype IA1 can act as a trigger for the comedo switch. Unlike commensal strains, phylotype IA1 has high lipase activity, hydrolyzing sebum triglycerides into free fatty acids, specifically palmitic acid. This metabolite stimulates LRIG1+ progenitors, inducing inflammation and initial comedo formation. The review discusses phylotypes, emphasizing known virulence factors of IA1, such as enhanced biofilm formation. We evaluate the efficacy and limitations of both old and new antibacterials, noting how newer materials that selectively remove IA1 can reduce non-inflammatory acne lesions, supporting a key role for this phylotype in the pathogenesis of acne.

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