Toxin-Producing Bacteria Induces Inflammation on Skin


The researchers at Johns Hopkins report the discovery of a key underlying immune mechanism causing skin inflammation. They explained the mechanism underlying inflammation in skin conditions such as atopic dermatitis (eczema). The study was published in Cell Host & Microbe.

Lloyd Miller is an associate professor of dermatology at the Johns Hopkins University School of Medicine. He said, “Our skin is covered with bacteria as part of our normal skin microbiome. It serves as a barrier that protects us from infection and inflammation. However, damage to the barrier increases exposure to certain bacteria and causes problems.”

The skin infection is usually caused by the bacteria Staphylococcus aureus (S. aureus). About 85% of individuals come into contact with S. aureus, while 20-30% of the U.S. population had S. aureus on their skin or in their nose. Eczema affected 20% of children and about 5% of adults, among which 90% had exceedingly high numbers of S. aureus bacteria on their inflamed skin, added Miller.

The cause of atopic dermatitis was not known, and there were no many good treatments available, said Miller. Thus, with his team, Miller works on understanding the mechanism so that new treatment could be developed.

In earlier studies, researchers had shown that generalized pustular psoriasis was caused by a genetic mutation. It is a rare disease in which the genetic mutation resulted in the unrestrained activity of a protein IL-36. This provided a hint that IL-36 was involved in inducing inflammation by bacteria on the skin surface, said Miller.

In the current study, the Miller's team experimented on two mice, one normal and the other was genetically engineered to lack the receptor for IL-36. Then, they soaked a small gauze pad with S. aureus and applied it to the back skin of the two mice. On examining, they found that the normal mice developed scaly and inflamed skin while the genetically engineered mice were free from skin inflammation.

Toxin-producing bacteria on skin surface induces a protein which caused the cells to react and cause inflammation

Miller and team were excited about the results. Currently, only a single biologic treatment targeting an inflammatory mechanism in atopic dermatitis was available in the market. Certain patients had treatment failures; thus, these would be benefited if there were biologics which targeted alternative mechanisms involved in skin inflammation.