VIENNA — Levels of some of the skin's key innate antimicrobial peptides are abnormally low in atopic dermatitis patients, perhaps accounting for the high rate of bacterial and viral superinfections in this population, Jurgen Harder, M.D., said at the annual meeting of the European Society for Dermatological Research.
The explanation for the low skin levels of antimicrobial peptides may lie in the high levels of Th2 cytokines typically present in atopic skin. These cytokines appear to sharply inhibit secretion of the antimicrobial peptides by keratinocytes, added Dr. Harder of the University of Kiel (Germany). He presented evidence from in vitro studies done in Kiel showing that high concentrations of the Th2 cytokines interleukin-4 (IL-4), IL-10, and IL-13 greatly dampen the normally robust induction of an important antimicrobial peptide in normal skin, human β-defensin-2, by Pseudomonas aeruginosa.
Expression of human β-defensin-2 was reduced in response to P. aeruginosa by 80%-90% in keratinocytes exposed to high levels of IL-4, by 70%-80% with IL-13, and by 20%-30% with IL-10.
These laboratory findings are consistent with the hypothesis that bacterially mediated induction of human β-defensin-2 and other inducible antimicrobial proteins is disrupted in atopic dermatitis patients and that the culprit is high levels of the Th2 cytokines.
These studies also suggest a novel potential strategy for prevention of cutaneous superinfections in patients with atopic dermatitis: treatments aimed at decreasing the elevated Th2 cytokine levels, Dr. Harder said.
It's worth noting, he added, that levels of innate antimicrobial proteins are high in the skin of psoriasis patients. This might explain their relatively low rate of bacterial superinfections despite the often severe damage to the skin's barrier function.