title: Characterization of spontaneous dermatitis in beige rats with IgE hyperproduction.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a common skin disease characterized by chronic recurrent eczematous lesions, but its exact etiology and mechanism are unclear. We found that beige rats (DAbg/bg), a mutant model of Chediak-Higashi syndrome, develop skin lesions characterized by pruritus, excoriation, erosion and alopecia. We describe the beige rat and examine its possible usefulness as an AD model.
  
  
  METHODS
  Beige rats of 4, 8, 13, 16, 26 and 52 weeks were used. Histological analysis of the skin was performed. Plasma IgE and cytokines were measured. Th1 and Th2 cytokines and RANTES mRNA expression of skin and lymph nodes were evaluated. Passive cutaneous anaphylaxis (PCA) reactions were examined, and maximization tests were conducted.
  
  
  RESULTS
  Skin lesions begin to develop with increases in serum IgE levels and the expression of IL-4 mRNA in the lymph node and skin. Histologically, skin lesions are characterized by acanthosis, ulceration and inflammatory cell infiltration in the dermis. Inflammatory cells consist of CD3+, CD4+, ED1+, ED2+ and I-A+ mononuclear cells, eosinophils, degranulated mast cells and neutrophils accompanying interleukin (IL)-4, interferon (IFN)-gamma and RANTES mRNA expressions of the skin. Inflammatory cells are reduced during chronification with decreased expressions of IL-4, IFN-gamma and RANTES mRNA. In addition, the rats show a high sensitivity to PCA reactions and maximization tests.
  
  
  CONCLUSIONS
  Our results show that some of the skin lesions of beige rats are morphologically similar to human AD, being characterized by inflammatory cell composition in the acute phase, and increased IgE and RANTES levels. However, the inflammatory process and cytokine expression pattern are different from those in human AD.
authors.affiliation: Research Institute of Drug Safety, Setsunan University, Hirakata, Japan. ozaki@pharm.setsunan.ac.jp
authors.forename: Kiyokazu
authors.initials: K
authors.lastname: Ozaki
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Matsuura
authors.forename: Isao
authors.initials: I
authors.lastname: Narama
mesh_terms: D000818:Animals; D002609:Chediak-Higashi Syndrome / Q000235:genetics / Q000276:immunology / Q000662:veterinary*; D018946:Chemokine CCL5 / Q000096:biosynthesis / Q000235:genetics; D003872:Dermatitis / Q000235:genetics / Q000276:immunology* / Q000473:pathology*; D003876:Dermatitis, Atopic / Q000175:diagnosis; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D007376:Interleukin-2 / Q000096:biosynthesis / Q000097:blood; D015847:Interleukin-4 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D008198:Lymph Nodes / Q000276:immunology; D008297:Male; D008925:Mites / Q000276:immunology / Q000472:pathogenicity; D051381:Rats; D011922:Rats, Mutant Strains / Q000235:genetics* / Q000276:immunology; D012867:Skin / Q000276:immunology / Q000473:pathology
chemical_list: D018946:Chemokine CCL5; D007376:Interleukin-2; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma