The human body is constantly exposed to various environmental agents, from viruses to bacteria and fungi, but most of these microbial organisms cause little or no response from our skin, which is responsible for controlling and protecting us from external dangers.
Until now, researchers weren’t entirely sure how this happened and why skin he was not constantly alarmed and inflamed.
In a study published on May 21, 2021 a Scientific immunology, scientists at the University of California, San Diego School of Medicine, identify and describe two enzymes responsible for protecting overall skin and body health from countless possible microbial intruders. These enzymes, called histone deacetylases (HDAC), inhibit the body’s inflammatory response to the skin.
“We’ve discovered why we tolerate certain microbes that live on our skin, while the bacteria themselves would do us a lot of harm if we were exposed to any other part of the body,” said Richard Gallo, MD, Ph.D., Ima Gigli Distinguished Professor of Dermatology and president of the Department of Dermatology at the UC San Diego School of Medicine. “In our research, we identified enzymes that act on the chromosome of specific skin cells that provide immune tolerance on the part of the skin.
“Without these enzymes that would tell our cells to ignore certain bacteria, we would have a constant rash on the skin.”
Gallo and colleagues say the potential mechanism of how the environment can interact and alter cell function it is through epigenetic control of gene expression. Within skin cells, proteins called toll-like receptors (TLRs) allow cells to feel their surroundings and potential dangers.
In most organs, TLRs act as an alert system that triggers an inflammatory response to threats. But in skin cells, the two identified HDAC enzymes, HDAC8 and HDAC9, inhibit the inflammatory response.
“This is one of the first demonstrations of how the microbiome can interact with skin epigenetic factors and modulate skin behavior through the inflammatory response,” said George Sen, Ph.D., associate professor of dermatology and cellular and molecular medicine at UC San Diego School of Medicine. “Any environment we face can change a person’s specific response. Because this epigenetic change is reversible, unlike alterations in our DNA, we can control our skin. inflammatory response by targeting these enzymes. “
The research was initially conducted on mouse models in which HDAC8 and HDAC9 had been genetically eliminated. As a result, the skin of the mice could not tolerate microbial or viral exposures, leading to a higher immune reaction. The team then reproduced the findings with human cells in a culture dish.
Gallo said the work could change the way doctors treat certain types of skin inflammation or other dermatological conditions.
“This is a completely new way of thinking about regulating skin immunity,” Gallo said. “By altering HDAC activity, we’ve provided a possible way to explore and soothe unnecessary inflammation by working with the skin. cells themselves. In the future, drugs designed to activate or deactivate these enzymes could help treat skin diseases as an alternative to antibiotics. ”
Yu Sawada et al, Innate cutaneous immune tolerance is mediated by epigenetic control of MAP2K3 by HDAC8 / 9, Scientific immunology (2021). DOI: 10.1126 / sciimmunol.abe1935
University of California – San Diego
Citation: Superficial relationship: enzymes protect skin ignoring microbes and viruses (2021, May 21) retrieved May 21, 2021 at https://medicalxpress.com/news/2021-05-superficial-relationship-enzymes- skin-microbes.html
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