From Bacteria to Eczema: Johns Hopkins Team Studies How Inflammation Happens

The bacteria Staphylococcus aureaus lives on the skin of about one-third of adults, and almost everyone comes in contact with it at some point. So, why is this bacteria harmless for most of us but the cause of a debilitating, itchy red skin rash for a handful of people?

Researchers at Johns Hopkins School of Medicine set out to learn more about this bacteria and published their results this week in the journal Cell Host & Microbe. They haven’t answered all their questions, but they learned more about why some people who have the bacteria on their skin develop atopic dermatitis, known as eczema to most people.

“Our skin is covered with bacteria as part of our normal skin microbiome and typically serves as a barrier that protects us from the infection and inflammation. However, when that barrier is broken, the increased exposure to certain bacteria really causes problems,” Lloyd Miller, MD, PhD, associate professor of dermatology at Johns Hopkins, said in a statement.

The bacteria S. aureas turns out to be a big culprit in atopic dermatitis. While the condition only affects about 5% of adults, 90% of those who have it carry this particular bacteria in the skin. Miller and his research team had noted that another rare disease, pustular psoriasis, involved a genetic mutation that caused an overreaction of a protein called interleukin 36 (IL-36), which has been implicated in several skin diseases. Miller believed that IL-36 would likely have a role in atopic dermatitis, as well.

The team soaked pads with S. aureus bacteria and placed them on the back skin of 2 sets of mice: one normal set, and one that had been genetically engineered without the receptor for IL-36 that ignites the inflammatory response. Sure enough, the mice treated with the oversupply of bacteria developed inflamed, flaky skin, while those without the receptor had little or no skin inflammation.

Connecting the dots between bacteria and skin inflammation opens the door to additional treatment beyond the current biologic approved to treat atopic dermatitis, Miller said. While the arrival of dupliumab has made a difference for many patients, he said, there are still some who don’t respond. (The drug targetes IL-4 and IL-13 signaling.)

“It would be better if there biologics on the market that target alternative mechanisms involved in skin inflammation,” Miller said.

Reference

Liu H, Archer NK, Dillen CA, et al. Staphylococcus aureus epicutaneous exposure drives skin inflammation via IL-36-mediated T cell responses. Cell Host and Microbe, 2017; DOI: 10.1016/j.chom.2017.10.006.