Molecule in Skin May Link Eczema and Asthma

May 19 (HealthDay News) -- A substance secreted by eczema-damaged skin might trigger asthma in children, U.S. researchers suggest.

The theory comes from a study of mice with an eczema-like condition, which suggested that early treatment of eczema and inhibition of the trigger substance might help prevent asthma.

An estimated 50 percent to 70 percent of children with severe eczema, known as atopic dermatitis, develop asthma, compared with about 9 percent of children in the general population. In the United States, about 17 percent of children have eczema, although not all cases are severe.

The progression from eczema to asthma is called the atopic march.

"Over the years, the clinical community has struggled to explain atopic march," Raphael Kopan, a professor of developmental biology and dermatology at Washington University School of Medicine in St. Louis and an author of the study, said in a news release from the school.

"So, when we found that the skin of mice with an eczema-like condition produced a substance previously implicated in asthma, we decided to investigate further," Kopan said. "We found that the mice also suffered from asthma-like responses to inhaled allergens, implicating the substance, called TSLP, as the link between eczema and asthma."

The researchers found that TSLP (thylmic stromal lymphopoietin) is secreted by damaged skin to alert the body that the skin's protective barrier has failed. TSLP activates an immune response that fights invaders.

"We are excited, because we've narrowed down the problem of atopic march to one molecule," Kopan said. "We've shown that skin can act as a signaling organ and drive allergic inflammation in the lung by releasing TSLP. Now, it will be important to address how to prevent defective skin from producing TSLP."

"If that can be done," she said, "the link between eczema and asthma could be broken."

The study appears May 19 in the journal PLoS Biology.


SOURCE: Washington University School of Medicine in St. Louis, news release, May 18, 2009

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