**5. Involvement of prostanoids in the pathogenesis of AD: Analysis based on animal models of AD**

As mentioned above, there are multiple pathogenetic factors of AD, but the skin barrier dysfunction and Th2 mediated immune response are its general characteristic features. Mouse ovalbumin (OVA)-induced dermatitis is one of the most frequently used AD models (He et al.; Spergel et al., 1998). In a typical mouse OVA-induced AD model, mice are first sensitized with an OVA patch using a transparent bio-occlusive dressing on a shaved and tape-stripped area of skin for one week. This sensitization to OVA is repeated in two-week intervals. After three to four sensitization cycles, the mice show elevated serum IgE and significant eosinophil and Th2-deviated lymphocyte infiltration in the skin, which is similar to the pathology of AD. In this model, COX-2 deficient mice and the administration of COX-2 inhibitor both showed enhanced eosinophil infiltration and elevated IL-4 expression in the skin lesion with elevated serum IgE and IgG1 (Laouini et al., 2005). These results suggest that COX-2-derived prostanoids play regulatory roles in the development of AD, such as Th differentiation and inflammatory cell infiltration in the skin. In the following sections, we will discuss how prostanoids are involved in Th differentiation, DC function, and inflammatory cell infiltration in skin immunity.
