Antimicrobial Peptide Loss, Except for LL-37, is not Characteristic of Atopic Dermatitis

Atopic dermatitis is an inflammatory skin disease characterized by significant permeability barrier damage. Regulation and maintenance of permeability and antimicrobial skin barriers are strongly connected. There is a lack of comprehensive studies of the expression of all 5 major antimicrobial peptide functional groups in atopic dermatitis. The aim of this study was to investigate the major antimicrobial peptide functional groups in lesional atopic dermatitis, non-lesional atopic dermatitis, and healthy control samples, using real-time quantitative PCR and immunohistochemistry. Lesional psoriatic skin was also examined as a diseased control. No differences in mRNA levels were detected between non-lesional atopic dermatitis and healthy control skin, and, at the protein level, the only change was the significantly decreased LL-37 in non-lesional atopic dermatitis. In lesional atopic dermatitis, several antimicrobial peptides were significantly altered at the mRNA level, while, at the protein level, all antimicrobial peptides were significantly upregulated or unchanged, except for LL-37, which decreased, compared with healthy controls. Antimicrobial peptides were similarly elevated in lesional atopic dermatitis and lesional psoriatic skin, with somewhat higher expression in lesional psoriatic skin, except for LL-37. In conclusion, LL-37 was the only antimicrobial peptide that was impaired in both non-lesional and lesional atopic dermatitis, highlighting its potential pathogenetic or exacerbating role in the initial stages of the disease. SIGNIFICANCE Data regarding antimicrobial peptides in atopic dermatitis are incomplete, and many discrepancies exist, which may be because the expression of antimicrobial peptides has often been compared with psoriatic rather than control skin. This study comprehensively analysed the main antimicrobial peptide representatives, at both the mRNA and protein levels, in clinically asymptomatic and symptomatic skin from patients with atopic dermatitis, and examined diseased control (psoriatic) and healthy control samples. The facts that the only impairment was a lack of induction of LL-37, and that LL-37 is associated with all the major pathogenic features of atopic dermatitis, indicate a driver role for LL-37 in the pathophysiology of atopic dermatitis, and raise the possibility of its therapeutic potential.