A study published last week in Cell Host & Microbe by researchers from Johns Hopkins describes a key underlying immune mechanism that explains how skin becomes inflamed from conditions such as atopic dermatitis, more commonly known as eczema.
Bacteria on the surface of our skin produce toxins which induce 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. However, when that barrier is broken, the increased exposure to certain bacteria really causes problems,” says Lloyd Miller, MD, PhD, associate professor of dermatology at the Johns Hopkins University School of Medicine.
Previous research showed a rare disease called generalized pustular psoriasis was caused by a genetic mutation that resulted in the unrestrained activity of IL-36, a protein normally produced in our skin. Miller and his team sought to determine whether IL-36 might be implicated in how bacteria on the skin might cause inflammation.
They applied gauze soaked in S. aureus to the backs of normal mice and mice genetically engineered to lack normal IL-36 activity. Miller’s team found the normal mice developed scaly and inflamed skin, and the genetically engineered mice lacking IL-36 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. 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,” says Miller.
Eczema can lead to other food allergies and other allergic conditions, including asthma, seasonal allergies and conjunctivitis. Blocking the skin inflammation in eczema has the potential to prevent these conditions.
- Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses – Cell Host & Microbe
- How the Skin Becomes Inflamed – John Hopkins Press Release