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The human body is constantly exposed to various environmental celebrities, from viruses to bacteria to fungi, but the majority of these parasitic organisms provoke little if any response from our skin, which is charged with monitoring and shielding from external dangers.
Until now, researchers weren’t quite sure how that happened — and why our skin wasn’t constantly alarmed and inflamed.
In a study published May 21, 2021 in Science Immunology, scientists at University of California San Diego School of Medicine identify and describe two enzymes responsible for protecting our skin and body’s overall health from countless potential microbial intruders. These enzymes, called histone deacetylases (HDACs), inhibit the body’s inflammatory reaction in the skin.
“In our research, we identified enzymes which act on the chromosome of specific skin cells that offer immune tolerance by the epidermis.
This is one of the first demonstrations of how the microbiome can interact with epigenetic factors in the skin and modulate the skin’s behavior through the inflammatory response. Whatever environment we’re facing can change a person’s specific response to it. Since this epigenetic change is reversible, unlike alterations to our DNA, we can potentially control our skin inflammatory response through targeting of these enzymes.”
George Sen, PhD, Associate Professor of Dermatology and Cellular and Molecular Medicine, UC San Diego School of Medicine
“Without these enzymes telling our cells to dismiss certain bacteria, we’d have a constant rash on the skin.”
Gallo and colleagues say the possible mechanism for how the environment can interact and alter cell function is through epigenetic control of gene expression. Within the skin cells, proteins known as toll-like receptors (TLRs) permit the cells to sense their environment and possible dangers.
In most organs, TLRs act as a warning system which triggers an inflammatory response to threats. However, in skin cells, both recognized HDAC enzymes, HDAC8 and HDAC9, inhibit the inflammatory response.
The research was originally conducted in mouse models in which HDAC8 and HDAC9 was genetically knocked out. As a result, the mice’s skin couldn’t tolerate microbial or viral ailments, resulting in a heightened immune response. The group then replicated the findings with individual cells in a culture dish.
Gallo said the work could change how doctors treat certain kinds of skin inflammation or other dermatologic conditions.
“This is a totally new way to think about skin immune regulation,” said Gallo. “Through alterations in HDAC activity, we have provided a possible way to explore and silent down unnecessary inflammation by working with skin cells themselves. In the future, drugs designed to turn these enzymes on or off may help treat skin disease as a substitute for antibiotics.”
University of California – San Diego