The study looked at whether people with atopic dermatitis have lower natural levels of the skin‑protective peptide LL‑37 (and a similar peptide, hBD‑2) in skin that looks normal. It found that, in non‑lesional skin, the amounts of LL‑37, hBD‑2 and the signaling molecule IL‑1α are about the same as in people without atopy, meaning the baseline skin defense isn’t reduced.

Recurrent skin infection is one of the major complications of atopic dermatitis and can be partly explained by decreased expression of antimicrobial peptides such as human beta-defensin-2 and cathelicidin (LL-37). In the human epidermis, human beta-defensin-2 is packed in the lamellar body and LL-37 is co-localized with intercellular lipid lamellae of the stratum corneum; together, these antimicrobial peptides constitute the primary defense system. IL-1alpha, a potent inducer of LL-37 and human beta-defensin-2, is also secreted from the disrupted epidermis for barrier homeostasis. In this study, we investigated whether expression of human beta-defensin-2 and LL-37 is constitutively decreased in the skin of atopic individuals. Nonlesional foreskins from atopic (n=7) and nonatopic (n=7) individuals were analyzed. The expression of LL-37, human beta-defensin-2 and IL-1alpha was analyzed using immunohistochemical staining, Western blot, and real-time polymerase chain reaction. Lamellar body density and secretion were evaluated by electron microscope. Quantitative analysis showed that the expression of each parameter was not significantly different between groups. Thus, basal expression of LL-37 and human beta-defensin-2 was not changed in atopic individuals. These results indicate that the expression of antimicrobial peptides at baseline was not different between nonlesional skin of atopic individuals and normal skin of nonatopic individuals.