中华皮肤科杂志 ›› 2016, Vol. 49 ›› Issue (10): 754-757.

• 综述 • 上一篇    

皮肤微生物群与特应性皮炎

苏惠春1,姚煦2,王宝玺3   

  1. 1. 中国医学科学院北京协和医学院皮肤病研究所博士
    2. 南京 中国医学科学院北京协和医学院皮肤病研究所
    3. 中国医学科学院北京协和医学院皮肤病研究所
  • 收稿日期:2015-12-02 修回日期:2016-02-15 出版日期:2016-10-15 发布日期:2016-09-30
  • 通讯作者: 姚煦 E-mail:dryao_xu@126.com
  • 基金资助:

    国家自然科学基金:C型凝集素受体DC-SIGN在特应性皮炎免疫异常中的作用和分子机制;国家自然科学基金:C型凝集素受体Langerin介导变应原多糖抗原免疫应答及其在特应性皮炎经皮致敏中的作用机制研究;国家自然科学基金:Langerin介导的靶向朗格汉斯细胞的尘螨纳米疫苗诱导免疫耐受防治特应性皮炎的研究;亚美医学基金会基金(MMAAP);江苏省自然科学基金:Langerin介导的靶向朗格汉斯细胞的尘螨纳米疫苗诱导免疫耐受防治特应性皮炎的研究

Skin microbiome and atopic dermatitis

SU HuiChun1, WHANG Baoxi   

  • Received:2015-12-02 Revised:2016-02-15 Online:2016-10-15 Published:2016-09-30

摘要:

皮肤的微生物群与机体保持着稳态关系,影响皮肤的屏障和免疫功能。皮肤微生物群的构成受多种因素的影响,具有多样性和特异性。以金黄色葡萄球菌为优势菌和皮肤微生物群的多样性降低是特应性皮炎的主要特点。金黄色葡萄球菌的过度繁殖 加重了特应性皮炎的炎症反应。表皮葡萄球菌虽然也是特应性皮炎优势菌,但通过树突细胞、分泌IL?17A的Th17细胞/IL?17通路调节皮肤屏障免疫反应,拮抗金黄色葡萄球菌过度繁殖,发挥保护性免疫防御作用。马拉色菌可以通过定植、致敏和交叉反应等多种机制诱导和加重特应性皮炎的炎症反应。皮肤益生菌的研究有望为特应性皮炎的治疗提供新的方向。

Abstract:

Su Huichun, Yao Xu, Wang Baoxi Department of Allergy and Rheumatology, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing 210042, China (Su HC, Yao X); Department of Dermatology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100144, China Corresponding authors: Yao Xu, Email: dryao_xu@126.com; Wang Baoxi, Email: wangbx@ncstdlc.org 【Abstract】 Skin microbiome maintain homeostasis with the host, and affect skin barrier and immune function. The components of skin microbiome are diverse and specific, and are affected by multiple factors. The predominance of Staphylococcus aureus and decrease in diversity of skin microbiome are a characteristic of atopic dermatitis. The overgrowth of S. aureus can aggravate inflammatory reactions in AD. S. epidermidis, although another predominant bacterium in AD, exerts an immunoprotective role by regulating skin barrier-associated immunoreactions through the dendritic cells, interleukin (IL)-17A-producing Th17 cells/IL-17 pathway, and by suppressing the overgrowth of S. aureus. Malassezia can induce and aggravate inflammatory reactions in AD through colonization, sensitization, cross reactions, and other mechanisms. Studies on skin probiotics may provide new directions for the treatment of AD.