Exacerbation of Atopic Dermatitis by Staphylococcal Colonization

DOI
  • Iwatsuki Keiji
    Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
  • Oono Takashi
    Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
  • Yamasaki Osamu
    Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

Bibliographic Information

Other Title
  • アトピー性皮膚炎を難治化させる黄色ブドウ球菌定着・感染症

Abstract

Staphylococcus colonization is one of the aggravating factors in patients with atopic dermatitis. The Th2 inflammatory response and persistent IL-18 secretion from keratinocytes is induced by wall TA and protein A, respectively. Staphylococcus enterotoxins A (SEA) and B (SEB) stimulate the expression of ICAM-1 and HLA-DR in normal human keratinocytes, and more than half of patients with atopic dermatitis have specific IgE antibodies to SEA and/or SEB in their serum. Epicutaneous sensitization with SEB elicites a local, cutaneous inflammatory response characterized by dermal infiltration with eosinophils and mononuclear cells, and induces mRNA expression of the Th2 cytokine, IL-4 without increased expression of the Th1 cytokine, IFN-γ. Epicutaneous exposure to superantigens skews the immune response toward Th2, leading to allergic skin inflammation and increased IgE synthesis. Patients with atopic dermatitis have significantly increased numbers of regulatory T (Treg) cells with normal immunosuppressive activity. However, after superantigen stimulation, Treg cells lose their immunosuppressive activity. S.aureus, therefore, may aggravate atopic dermatitis by immunomudulatory effects of the cell components and exotoxins. Neither antimicrobial nor antiseptic treatment is effective for eradication of colonizing S.aureus in the horny layers covered with biofilm.

Journal

  • Hifu no kagaku

    Hifu no kagaku 5 (Suppl.7), B29-B32, 2006

    Meeting of Osaka Dermatological Association/Meeting of Keiji Dermatological Association

Details 詳細情報について

  • CRID
    1390282680165414016
  • NII Article ID
    130004934485
    130005404770
  • DOI
    10.11340/skinresearch.5.suppl.7_b29
  • ISSN
    18839614
    13471813
  • Text Lang
    ja
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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