Glyoxal-induced exacerbation of pruritus and dermatitis is associated with staphylococcus aureus colonization in the skin of a rat model of atopic dermatitis.

Atopic dermatitis (AD) is a chronically relapsing inflammatory disease resulting from complex interactions between immunological and environmental factors [1]. Immunological features, including barrier dysfunction and type 2 T-helper cell (Th2) immune reactions, form the basis for initiation of AD pathology. Accordingly, acute lesions in the skin of patients with AD are characterized by profound increment of Th2 cytokines such as interleukin (IL)-4 and IL-5 [2], whereas in chronic AD lesions, type 1 T-helper cell (Th1) immune reaction coexists with Th2 immune reaction rather than a switch to Th1-dominant inflammation [3–5].