Animal models of atopic dermatitis

Abstract

Atopic dermatitis (AD) is characterized by allergic skin inflammation. A hallmark of AD is dry itchy skin due, at least in part, to defects in skin genes that are important for maintaining barrier function. The pathogenesis of AD remains incompletely understood. Since the description of the Nc/Nga mouse as a spontaneously occurring model of AD, a number of other mouse models of AD have been developed. They can be categorized into three groups: (1) models induced by epicutaneous application of sensitizers; (2) transgenic mice that either overexpress or lack selective molecules; (3) mice that spontaneously develop AD-like skin lesions. These models have resulted in a better understanding of the pathogenesis of AD. This review discusses these models and emphasizes the role of mechanical skin injury and skin barrier dysfunction in eliciting allergic skin inflammation.

Figure 1

EC sensitization protocol. Mice were sensitized with OVA (100 μg) or saline applied in 100 μl to a sterile patch. The patch was placed for a one-week period, then removed. Two weeks later, an identical patch was reapplied to the same skin site. Each mouse had a total of three one week exposures to patch separated from each other by two week intervals. All experiments are done at the end of the third sensitization.

Figure 2

Histological features of OVA and saline-sensitized skin sites in BALB/c mice. Skin sections were stained with H&E and examined at 200× and 400× magnification. There is marked hyperplasia of the epidermis, a dermal infiltrate and mild spongiosis. The cellular infiltrate consists of neutrophils, eosinophils and lymphocytes. Further magnification in the insert (bold bordered box) shows the presence of the multiple eosinophils.

Figure 3

Scheme for testing the effect of tape stripping on DC polarity.