Li X M, Kleiner G, Huang C K, Lee S Y, Schofield B, Soter N A, Sampson H A
Department of Pediatrics, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029-6574, USA.
J Allergy Clin Immunol. 2001 Apr;107(4):693-702. doi: 10.1067/mai.2001.114110.
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(+) T(H)2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD.
The purpose of this study was to establish a murine model of food-induced AD.
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.
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.
This eczematous eruption resembles AD in human subjects and should provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD.
特应性皮炎（AD）是一种湿疹样皮肤疹，通常始于婴儿早期，影响高达12%的人群。尽管它常常是特应性疾病的首个症状，其特征为血清IgE水平升高、嗜酸性粒细胞增多以及早期以海绵形成和CD4(+) T(H)2细胞浸润为特征的组织学改变，但这种疾病的病因尚未完全明确。食物过敏被认为是高达40%的中重度AD患儿的一个致病因素。
本研究的目的是建立食物诱导的AD小鼠模型。
用霍乱毒素佐剂对雌性C3H/HeJ小鼠进行牛奶或花生口服致敏，然后使其接触低剂量变应原。对皮肤病变进行组织学检查、检测变应原特异性血清Ig水平以及变应原诱导的T细胞增殖和细胞因子产生情况。
在低剂量接触牛奶或花生蛋白后，约三分之一的小鼠出现了湿疹样皮疹。外周血嗜酸性粒细胞增多以及血清IgE水平升高。对病变皮肤的组织学检查显示有海绵形成以及由CD4(+)淋巴细胞、嗜酸性粒细胞和肥大细胞组成的细胞浸润。IL-5和IL-13 mRNA表达仅在出现湿疹样皮疹的小鼠皮肤中升高。外用糖皮质激素治疗皮疹可减轻瘙痒并使皮疹消退。
这种湿疹样皮疹与人类特应性皮炎相似，应为研究特应性皮炎中食物过敏的免疫致病机制提供一个有用的模型。
