Marsella Rosanna, Samuelson Don
Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.
Vet Dermatol. 2009 Oct;20(5-6):533-40. doi: 10.1111/j.1365-3164.2009.00809.x.
Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease caused by complex interactions between genetics and environmental factors. In human beings, impairment of the skin barrier is demonstrated and thought to be responsible for enhanced penetration of allergens and increased risk for allergic sensitization. Once inflammation is triggered, further impairment of the skin barrier occurs, leading to self-perpetuating cycles of sensitizations. Canine AD appears to share many similarities with the human counterpart, clinically and immunologically. It is hypothesized that a primary defect of skin barrier function also exists in subsets of atopic dogs (e.g. in an experimental model using high IgE-producing beagles), particularly in young dogs, and in sites predisposed to the development of lesions. This impairment is present in clinically normal skin, worsens with development of lesions and can be quantified by measurement of transepidermal water loss. Therefore, the distribution of lesions in AD may be linked to a primary skin barrier defect in those sites and not simply due to contact with allergens, and increased susceptibility to penetration of allergen may exist early in life. Ultrastructurally, transmission electron microscopy reveals that clinically normal skin in atopic dogs has abnormalities in lamellar body secretion and extracellular lamellar bilayer structure when compared with normal dogs. Development of lesions worsens these changes (e.g. widening of intercellular spaces, release of lamellar bodies, and disorganization of lipid lamellae). It is proposed that the paradigm of canine AD as primarily due to immunologic aberration ('inside/outside') should be shifted to include a primary defect in barrier function ('outside/inside').
特应性皮炎（AD）是一种由遗传和环境因素复杂相互作用引起的慢性复发性炎症性皮肤病。在人类中，皮肤屏障受损已得到证实，并被认为是过敏原穿透增强和过敏致敏风险增加的原因。一旦炎症触发，皮肤屏障会进一步受损，导致致敏的自我持续循环。犬特应性皮炎在临床和免疫方面似乎与人类特应性皮炎有许多相似之处。据推测，特应性犬的某些亚群（例如在使用高IgE产生的比格犬的实验模型中），特别是幼犬以及易发生病变的部位，也存在皮肤屏障功能的原发性缺陷。这种损伤存在于临床正常皮肤中，随着病变的发展而恶化，并且可以通过测量经表皮水分流失来量化。因此，特应性皮炎中病变的分布可能与这些部位的原发性皮肤屏障缺陷有关，而不仅仅是由于与过敏原接触，并且在生命早期可能就存在对过敏原穿透的易感性增加。在超微结构上，透射电子显微镜显示，与正常犬相比，特应性犬的临床正常皮肤在板层小体分泌和细胞外板层双分子层结构方面存在异常。病变的发展会使这些变化恶化（例如细胞间隙增宽、板层小体释放和脂质板层紊乱）。有人提出，犬特应性皮炎主要归因于免疫异常（“内/外”）的范式应转变为包括屏障功能的原发性缺陷（“外/内”）。
