Murine model of atopic dermatitis associated with food hypersensitivity

Background: Atopic dermatitis (AD) is an eczematous skin eruption that gene rally begins in early infancy and affects up to 126 of the population. The cause of this disorder is not fully understood, although it is frequently t he first sign of atopic disease and is characterized by an elevated serum I gE level, eosinophilia, and histologic tissue changes characterized early b y spongiosis and a CD4(+) T(H)2 cellular infiltrate. Hypersensitivity to fo ods has been implicated as one causative factor in up to 40% of children wi th moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of foo d-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 exp osure. Histologic examination of skin lesions, allergen-specific serum Ig l evels, and allergen-induced T-cell proliferation and cytokine production we re examined. Results: An eczematous eruption developed in approximately one third of mic e after low-grade exposure to milk or peanut proteins. Peripheral blood eos inophilia and elevated serum IgE levels were noted. Histologic examination of the Lesional skin revealed spongiosis and a cellular infiltrate consisti ng 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 erupti on. 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 sho uld provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD.