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 β-defensin-2 and cathelicidin (LL-37). In the human epidermis, human β-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-1α, a potent inducer of LL-37 and human β-defensin-2, is also secreted from the disrupted epidermis for barrier homeostasis. In this study, we investigated whether expression of human β-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 β-defensin-2 and IL-1α 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 β-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.
All Science Journal Classification (ASJC) codes
- Pediatrics, Perinatology, and Child Health