Murine model of atopic dermatitis associated with food hypersensitivity

• Published in: Journal of allergy and clinical immunology 2001-04, Vol.107 (4), p.693-702
• Main Authors: Li, Xui-Min, Kleiner, Gary, Huang, Chin-Kang, Lee, Soo Yung, Schofield, Brian, Soter, Nicholas A., Sampson, Hugh A.
• Format: Article
• Language: English
• Subjects: Allergic diseases; Animals; Atopic dermatitis; Biological and medical sciences; Dermatitis, Atopic - etiology; Dermatitis, Atopic - microbiology; Dermatitis, Atopic - pathology; eczema; Eosinophils - physiology; Female; food hypersensitivity; Food Hypersensitivity - complications; Hypersensitivity, Immediate; IgE-mediated hypersensitivity; Immunoglobulin E - blood; Immunopathology; Interleukin-4 - genetics; Lymphocyte Activation; Medical sciences; Mice; Mice, Inbred C3H; Milk Hypersensitivity - immunology; murine model; RNA, Messenger - analysis; Skin allergic diseases. Stinging insect allergies; T-Lymphocytes - immunology; TH2-like cytokines
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1067/mai.2001.114110

Background: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 12% of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4+ TH2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of food-induced AD. Methods: Female C3H/HeJ mice were sensitized orally to cow’s milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. Results: An eczematous eruption developed in approximately one third of mice after low-grade exposure to milk or peanut proteins. Peripheral blood eosinophilia and elevated serum IgE levels were noted. Histologic examination of the lesional skin revealed spongiosis and a cellular infiltrate consisting of CD4+ lymphocytes, eosinophils, and mast cells. IL-5 and IL-13 mRNA expression was elevated only in the skin of mice with the eczematous eruption. Treatment of the eruption with topical corticosteroids led to decreased pruritus and resolution of the cutaneous eruption. Conclusion: This eczematous eruption resembles AD in human subjects and should provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD. (J Allergy Clin Immunol 2001;107:693-702.)