The human body is constantly exposed to various environmental actors, from viruses to bacteria to fungi, but most of these microbial organisms provoke little or no response from our skin, which is charged with monitoring and protecting 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 response in the skin.
"We have figured out why we tolerate certain microbes living on our skin, while the same bacteria would make us very sick if exposed elsewhere in the body," said Richard Gallo, MD, Ph.D., Ima Gigli Distinguished Professor of Dermatology and chair of the Department of Dermatology at 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 by the skin.
"Without these enzymes telling our cells to ignore certain bacteria, we'd have a constant rash on our skin."
Gallo and colleagues say the potential mechanism for how the environment can interact and alter cell function is through epigenetic control of gene expression. Within the skin cells, proteins called toll-like receptors (TLRs) allow the cells to sense their surroundings and potential dangers.
In most organs, TLRs act as a warning system that triggers an inflammatory response to threats. But in skin cells, the two identified HDAC enzymes, HDAC8 and HDAC9, inhibit the inflammatory response.
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