4.4 Review

Staphylococcus aureus in atopic dermatitis: Strain-specific cell wall proteins and skin immunity

期刊

ALLERGOLOGY INTERNATIONAL
卷 68, 期 3, 页码 309-315

出版社

JAPANESE SOCIETY ALLERGOLOGY
DOI: 10.1016/j.alit.2019.02.006

关键词

Atopic dermatitis; Cell wall protein; Clonal complex; Microbiome; Staphylococcus aureus

资金

  1. Japan Society for the Promotion of Science, Japan [18K16031]
  2. Novartis Research Grants 2018, Japan
  3. Tsuchiya Foundation 2018, Japan
  4. Japanese Society of Allergology
  5. Grants-in-Aid for Scientific Research [18K16031] Funding Source: KAKEN

向作者/读者索取更多资源

Atopic dermatitis (AD) is a common chronic skin disease. The presence of the bacterium Staphylococcus aureus (S. aureus) is frequently detected on skin affected with AD. In this review, we focused on the characteristics of S. aureus strains isolated from AD skin, particularly the proteins on the cell surface that modulates the interactions between Langerhans cell, keratinocyte, and S. aureus. The skin microbiome plays an important role in maintaining homeostasis of the skin, and colonization of S. aureus in AD is considered to be deeply involved in the clinical manifestation and pathogenesis of skin flares. Colonizing S. aureus strains in AD harbor different surface proteins at the strain level, which are indicated as clonal complexes. Moreover, the cell wall proteins of S. aureus affect skin adhesion and induce altered immune responses. S. aureus from AD skin (AD strain) exhibits internalization into keratinocytes and induces imbalanced Th1/Th2 adaptive immune responses via Langerhans cells. AD strain-derived cell wall proteins and secreted virulence factors are expected to represent therapeutic targets. In addition, the microbiome on the AD skin surface is associated with skin immunity; thus, microbiome-based immunotherapy, whose mechanism of action completely differs from that of typical steroid ointments, are expected to be developed in the future. Copyright (C) 2019, Japanese Society of Allergology. Production and hosting by Elsevier B.V.

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