Atopic dermatitis (AD) is a chronic skin disease with a prevalence of 10%–20% in children and 1%–3% in adults.1 We investigated the expression patterns of interleukin (IL)-1α, IL-1β and IL-18 in AD and their interplay with the expression of profilaggrin, loricrin and claudin-1.
We performed analyses by RT-qPCR and immunohistochemistry using skin samples from AD patients (n = 6) and healthy controls (HC) (n = 6), but also human skin explants (n = 4–8). Non-atopic, HCs were defined as having no personal or family history of allergic diseases, no personal history of chronic systemic or skin diseases and a serum total IgE that was ≤2 SD of age-dependent norms. SCORAD and three item severity scores were used to evaluate the severity of AD. Punch biopsies were obtained from forearm of six AD patients and six HC. Innate immune responses derived from keratinocytes are important initiators of skin inflammation, for example after skin irritation.2 The role of IL-1 cytokines including IL-1α, IL-1β and IL-18 in skin inflammation has been established for a long time.3 We observed enhanced IL-1α and IL-1β positive cells in lesional—compared to non-lesional skin (Figure 1a,b). Also, IL-1β- and IL-18-positive cells were upregulated in lesional AD compared to HC (Figure 1b,c).
