Researchers from Johns Hopkins University School of Medicine have discovered a previously unknown immune mechanism that can provoke inflammation of the skin from conditions including atopic dermatitis (eczema). This mechanism involves activation of a protein by commonly present Staphylococcus aureus bacteria on the skin that causes an inflammatory reaction. Study author Lloyd Miller, MD, PhD, associate professor of dermatology at Johns Hopkins, commented, “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.” The findings were published online last week in the journal Cell Host and Microbe.
Eczema, an inflammatory skin disease, affects some 20% of children and 5% of adults. Building on past research into a rare disease called generalized pustular psoriasis, the Johns Hopkins team hypothesized that unchecked activity of the protein IL-36 might also be implicated in the inflammatory process in eczema. Working with mouse models, they applied Staphylococcus aureus to normal mice and to mice that were genetically engineered to lack the receptor for IL-36. The normal mice developed inflamed and scaly skin, while the IL-36 deficient cohort did not. Dr. Miller stated “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.”
Read more about the discovery.
The journal abstract may be read here.
Posted on November 13, 2017