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Article
Pinpointing S. aureus as AD perpetrator
Orlando, Fla. — Poorly controlled atopic dermatitis (AD) may remain elusive to treatment, particularly if its pathogenesis is not understood. While it is known that the altered barrier of atopic skin provides a portal of entry for various pathogens, it is the skin inflammation in AD that reduces the ability of patients with atopy to fight infection, according to Donald Y. M. Leung, M.D., Ph.D., head of pediatric allergy-immunology at the National Jewish Medical and Research Center in Denver.
Recent research completed by Dr. Leung's laboratory supports previous work that shows Staphylococcal aureus (S. aureus) as a primary culprit of increased bacterial infection by secreting superantigens resulting in the worsening of skin inflammation in AD and the production of IgE antibodies to superantigens correlating with the severity of this skin disease. These findings may be the catalyst for change in how AD is treated.
"We have found that these superantigens induce steroid resistance," Dr. Leung says. "Therefore, superantigens may also complicate the treatment of atopic dermatitis."
"The absence of antimicrobial peptides predisposes patients with atopic dermatitis to increased bacterial and viral skin infections," Dr. Leung says. "New therapies will focus on strategies to boost expression of these antimicrobial peptides or replace the antimicrobial peptides that are deficient in atopic dermatitis. This may be made possible for producing drugs that mimic the action of antimicrobial peptides so that they may be applied to atopic skin infections or alternatively reducing the inflammatory molecules that inhibit production of antimicrobial peptides.
While it has been shown that the absence of certain antimicrobial peptides is linked to increased S. aureus and herpes skin infection, it has become apparent that these conditions are acquired as the result of the Th2 cytokine response in acute AD. Studies showing that the reversal of the deficient innate immune response by antibodies to IL-4 and IL-13 suggest a new therapeutic strategy in the treatment of AD, according to Dr. Leung's findings.
Dissecting S. aureus To further understand why those patients with AD are prone to infection, Dr. Leung will continue to scrutinize S. aureus in future studies.
"We are further characterizing the molecules produced by staph aureus, which contribute to allergic and inflammatory responses in atopic dermatitis," Dr. Leung says. "A better understanding (of why these patients are prone to infection) will point to new approaches for treatment of atopic dermatitis."
Although definitive science regarding S. aureus' impact on AD may take time to uncover, today's findings from Dr. Leung are an authoritative direction for dermatologists who manage the daily complications AD presents in their patients.
