title: Atopic dermatitis-like skin lesions induced by topical application of mite antigens in NC/Nga mice.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a chronic relapsing inflammation usually observed in patients with an individual or a familial history of atopic diseases, precipitated by environmental factors including mite antigens (Ag). However, the exact etiology of AD is unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is necessary. In this study, we developed a new animal model of AD induced by mite Ag in NC/Nga mice.
  
  
  METHODS
  We injected the extracts of mite Ag intradermally at the ventral side of the ear of SPF NC/Nga mice on days 0, 2, 4, 7, 9, 11, 14 and 16, and measured the clinical symptoms and the ear thickness. On day 18, we collected blood and submandibular lymph nodes (LN) of the immunized ear to perform a histochemical analysis, and to measure the plasma immunoglobulins and cytokines.
  
  
  RESULTS
  The NC/Nga mice immunized with mite Ag suffered from AD-like skin lesions including erythema followed by edema, excoriation and scaling. The histological and immunohistochemical examinations of the affected skin showed epidermal hyperplasia with hyperkeratosis, severe infiltration of CD4+ T lymphocytes, eosinophils and macrophages, and degranulation of mast cells. The total plasma IgE level was markedly elevated in mite Ag-treated mice. LN cells of mice immunized with mite Ag synthesized IgE in an Ag-dependent manner and secreted interleukin-4 (IL-4) and IL-5 but not interferon-gamma.
  
  
  CONCLUSIONS
  NC/Nga mice treated with mite Ag manifest clinical and immunological aspects similar to patients with AD, suggesting that this model is suitable for exploring the pathogenesis of human AD.
authors.affiliation: Department of Respiratory Diseases, Medical Biology Research Laboratories, Fujisawa Pharmaceutical Co. Ltd., 2-1-6 Kashima, Yodogawa-ku, Osaka, Japan. tatsuya_sasakawa@po.fujisawa.co.jp
authors.forename: T
authors.initials: T
authors.lastname: Sasakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Higashi
authors.forename: S
authors.initials: S
authors.lastname: Sakuma
authors.forename: Y
authors.initials: Y
authors.lastname: Hirayama
authors.forename: Y
authors.initials: Y
authors.lastname: Sasakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ohkubo
authors.forename: T
authors.initials: T
authors.lastname: Goto
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Matsuda
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D000941:Antigens / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes; D003876:Dermatitis, Atopic / Q000209:etiology / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008925:Mites / Q000276:immunology*
chemical_list: D000485:Allergens; D000941:Antigens; D007073:Immunoglobulin E