Johns Hopkins experts gain insight into underlying cause of eczema

Researchers at Johns Hopkins are reporting a discovery that explains why our skin becomes inflamed from conditions such as atopic dermatitis, more commonly known as eczema.

The bacteria Staphylococcus aureus, or S. aureus, is an important human pathogen and the most common cause of skin infections in people. In a study described online in Cell Host & Microbe, the scientists found that this common, toxin-producing bacteria sometimes induces a protein that causes our own cells to react and cause inflammation.

"Our skin is covered with bacteria as part of our normal skin microbiome and typically serves as a barrier that protects us from infection and inflammation," says Lloyd Miller, associate professor of dermatology at the Johns Hopkins University School of Medicine. "However, when that barrier is broken, the increased exposure to certain bacteria really causes problems,"

Twenty to 30 percent of the U.S. population have S. aureus living on their skin or in their nose, Miller adds, and over time, up to 85 percent of people come into contact with it.

Eczema is an inflammatory skin disease that affects 20 percent of children and about 5 percent of adults. Ninety percent of patients with eczema have exceedingly high numbers of S. aureus bacteria on their inflamed skin. Untreated eczema can lead to other allergic conditions, including asthma, food allergies, seasonal allergies, and conjunctivitis. Blocking the skin inflammation in eczema has the potential to prevent these unwanted conditions.

"We don't really know what causes atopic dermatitis, and there aren't many good treatments for it," says Miller.

His team set out to learn more about how the condition arises in hopes that other treatments can be developed.

Previous research had shown that a rare disease that causes the skin to erupt into pustules was caused by a genetic mutation that resulted in unrestrained activity of a protein normally produced in our skin. This, Miller says, was a clue that this same protein might have something to do with how bacteria on the skin surface induce inflammation.

The team tested this idea in mice by soaking a small gauze pad with S. aureus and applying it to the back skin of both normal mice and those that had been genetically engineered to lack the receptor for the protein that triggers inflammatory responses. Miller's team found the normal mice developed scaly and inflamed skin, and the genetically engineered mice lacking protein activity had almost no skin inflammation.

"We are very excited about these results as there is currently only a single biologic treatment targeting an inflammatory mechanism in atopic dermatitis on the market," Miller says. "As there are patients who don't respond or have treatment failures, it would be better if there were biologics on the market that target alternative mechanisms involved in skin inflammation."