Atopic Dermatitis Research Network (ADRN)

ADRN Research

The Atopic Dermatitis Research Network (ADRN) is a consortium of academic medical centers, established and funded by the National Institute of Allergy and Infectious Diseases (NIAID) since 2004.

 

Goals of ADRN

To understand more about the immune system and skin barrier of AD patients which may lead to new therapeutic targets that minimize the likelihood of cutaneous infections that frequently exacerbate this disease.

Atopic dermatitis patients are particularly prone to skin infections.  Up to 90 percent of patients have S. aureus that can be cultured from their skin, and 30 percent are prone to overt infections, which can cause both localized (e.g. pain, swelling and drainage) and systemic (e.g. fever, chills, fatigue) symptoms.

 

Scope of Research

The research is based on animal, human and in vitro (tissue culture) studies. Researchers in the ADRN will evaluate AD patients' genes, innate and adaptive immune responses and skin barrier to identify factors that make them susceptible to infections. The researchers also plan to conduct clinical trials using novel biologic therapy, microbiome treatment and mechanistic studies to understand the basis of eczema herpeticum and S. aureus infection including MRSA infections.

 

Current Research

 

Completed Research

In the first funding cycle the network conducted clinical studies in humans and mouse model systems to address why AD patients were more susceptible to viral skin infections and complications from exposure to the smallpox vaccine. Consortium investigators studied a group of individuals with both AD and a history of eczema herpeticum (eczema along with a widespread herpes simplex skin infection). 

Several important insights emerged from this first funding period and include the following:

  • There is a close relationship between AD and a skin barrier defect called filaggrin mutations.

  • Atopic individuals produce proteins in their skin that result in reduced expression of a key skin barrier protein called filaggrin.

  • Atopic dermatitis individuals who get eczema herpeticum have lower levels of naturally occurring antibiotics (antimicrobial peptides) and higher levels of the allergic protein, IgE, than those with AD alone.

  • These same individuals are more reactive to a number of environmental allergens and more likely to report a history of other atopic disorders such as asthma or food allergy.

  • Atopic dermatitis individuals who get eczema herpeticum also report more bacterial skin infections needing prescription systemic antibiotics.

  • Genetic markers have been identified that are different in AD individuals who get eczema herpeticum and those who do not get this viral skin infection, and healthy individuals without atopy.

  • S. aureus colonization and eczema herpeticum are associated with increased allergic responses

  • The microbiome of patients with AD are deficient in the production of antimicrobial proteins that play an important role in fight skin infection.

In the next five years, the consortium will conduct clinical research studies that will expand the focus to bacterial skin infections associated with AD.  The studies will focus on Staphylococcus aureus  infections distinguishing both antibiotic-resistant S. aureus and antibiotic-sensitive S. aureus  (MSSA) infections as well as widespread herpes simplex virus infections of the skin, both of which are more prevalent among AD patients.