痤疮丙酸杆菌通过辅助性T淋巴细胞17炎症通路致寻常痤疮的机制研究进展  

Research progress on mechanisms of Cutibacterium acnes inducing acne vulgaris via Th17 inflammatory pathway

作　　者：王羽侬 孙娅楠[2] 任星 周娜 王毅[2] WANG Yunong;SUN Yanan;REN Xing;ZHOU Na;WANG Yi(Department of Dermatology,the Third Affliated Hospital of Beijing University of Chinese Medicine,Beijing 100029,China)

机构地区：[1]北京中医药大学第三附属医院皮肤科,北京100029 [2]中国中医科学院医学实验中心

出　　处：《实用皮肤病学杂志》2024年第4期226-230,共5页Journal of Practical Dermatology

摘　　要：寻常痤疮是一种常见的慢性炎症性皮肤病,皮脂分泌旺盛、毛囊角化过度、皮肤菌群失调和局部免疫炎症反应是寻常痤疮发生的重要因素。近年来对痤疮发生机制的研究成果包括:痤疮丙酸杆菌(C.acnes)生物膜形成与体内毒力因子增强有关;C.acnes多样性下降,令ⅠA1型C.acnes占主导地位,从而诱导辅助性T淋巴细胞17(Th17)通路激活,角质形成细胞、成纤维细胞、单核细胞和皮脂细胞在痤疮炎症反应中发挥核心作用。该文就C.acnes诱发Th17炎症通路激活导致痤疮的发病机制进行综述。Acne vulgaris is a common chronic inflammatory skin disease.The important pathogenic factors of acne vulgaris include high sebum secretion,hyperkeratosis of hair follicles,dysregulation of skin flora and local immune inflammatory reaction.Recent studies on the mechanisms underlying acne occurrence have shown that the biofilm formation of Cutibacterium acnes(C.acnes)is related to increased in vivo virulence factors;The decline in C.acnes diversity led to the dominance of type IA1 C.acnes,subsequently inducing the activation of helper T cells 17(Th17)pathway.In addition,keratinocytes,fibroblasts,monocytes and sebum cells play pivotal roles in the inflammatory response of acne.In this paper,the pathogenesis of acne,triggered by the activation of Th17 inflammatory pathway induced by C.acnes,was comprehensively reviewed.

关 键 词：痤疮 痤疮丙酸杆菌 TH17细胞 炎症 发病机制 

分 类 号：R758.733[医药卫生—皮肤病学与性病学] R364.5[医药卫生—临床医学]