2. Academic Validation
  3. Extracellular Vesicles of Commensal Skin Microbiota Alleviate Cutaneous Inflammation in Atopic Dermatitis Mouse Model by Re-Establishing Skin Homeostasis

Extracellular Vesicles of Commensal Skin Microbiota Alleviate Cutaneous Inflammation in Atopic Dermatitis Mouse Model by Re-Establishing Skin Homeostasis

  • J Invest Dermatol. 2023 Mar 11;S0022-202X(23)00169-0. doi: 10.1016/j.jid.2023.02.023.
Hong Zhou 1,  Xi Tan 1,  Guozhong Chen 2,  Xinxin Liu 3,  Aiping Feng 3,  Zhi Liu 2,  Wei Liu 4
Affiliations

Affiliations

  • 1 National Engineering Research Center for Nanomedicine, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
  • 2 Department of Biotechnology, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
  • 3 Department of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 4 National Engineering Research Center for Nanomedicine, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China. Electronic address: wliu@hust.edu.cn.
PMID: 36907322 DOI: 10.1016/j.jid.2023.02.023
Abstract

Atopic dermatitis (AD) is a chronic inflammatory cutaneous disorder in which the skin is affected by microbial dysbiosis. The role of commensal skin microbiota in AD is of great interest. Extracellular vesicles (EVs) are important regulators of skin homeostasis and pathology. The mechanism of preventing AD pathogenesis through commensal skin microbiota-derived EVs remains poorly understood. In this study, we investigated the role of commensal skin bacterium Staphylococcus epidermidis-derived EVs (SE-EVs). We showed that SE-EVs significantly decreased the expression of proinflammatory genes (TNFα, IL1β, IL6, IL8, and iNOS) through lipoteichoic acid and increased the proliferation and migration of calcipotriene (MC903)-treated HaCaT cells. Furthermore, SE-EVs increased the expression of human β-defensins 2 and 3 in MC903-treated HaCaT cells through Toll-like Receptor 2, enhancing resistance to S. aureus growth. In addition, topical SE-EV application remarkably attenuated inflammatory cell infiltration (CD4+ T cells and Gr1+ cells), T helper 2 cytokine gene expression (Il4, Il13, and Tlsp), and IgE levels in MC903-induced AD-like dermatitis mice. Intriguingly, SE-EVs induced IL-17A+ CD8+ T-cell accumulation in the epidermis, which may represent heterologous protection. Taken together, our findings showed that SE-EVs reduced AD-like skin inflammation in mice and may potentially be a bioactive nanocarrier for the treatment of AD.

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