Some of the most powerful human experiences are universal. Love. Heartbreak. Elation. Hating acne. The microscopic jerk known as Propionibacterium acnes wreaks havoc on our skin, makes middle school harder, and can cause pain and scarring. Now scientists say we’re one step closer to understanding what makes acne so devious—and how we might conquer it. They published their findings in the journal Science Immunology.
Acne breakouts are the result of a perfect storm of disgusting conditions near the surface of your skin. Natural oils and dead cells build up around your hair follicles, creating the ideal environment for bacteria to breed. The resulting infection sets off your immune system, which leads to inflammation, redness, and those oh-so-delightful pustules on your face, neck, chest, back, or shoulders.
We knew all this already. What we didn’t know was how P. acnes, which ordinarily lives harmlessly on the skin, could multiply out of control—or how its little fortresses in your follicles send your immune system into such a panic.
Previous studies on the bacteria in the human gut have found that certain bacteria produce chemicals called short-chain fatty acids (SCFAs). These acids then block the action of an immune compound called histone deacetylase (HDAC). Suppressed HDAC can then lead to immune trouble and, from there, inflammation.
Dermatology and biochemists at the University of California, San Diego were curious to see if the same patterns would play out on and inside our skin. First, they simulated the greasy skin experience by culturing acne bacteria in Petri dishes full of blood cells or oil-producing skin cells. They ensured that the environment in the dish was smothering, starved of oxygen like the inside of a clogged follicle. Then they let it fester.
Once they had a good SCFA stew going, they ran the cultures through an RNA sequencer to see how the bacteria and cells were performing. They also applied SCFAs both on and just under the skin of lab mice to see how skin layers might react.
The team found that, as with gut cells, the skin cells could be goaded into inflammation by acne’s SCFA bullies. The same pattern bore out for the mice—but only on the topmost layer of keratinocytes, the most common type of epidermal cells. Exposing lower skin layers to acne and SCFA actually activated those cells’ immune systems, making it easier for them to fight off infection.
Adam Friedman teaches and researches dermatology at the George Washington University School of Medicine. He was unaffiliated with the study but praised the findings, telling mental_floss that they “unveil a new understanding of how P. acnes contributes to the pathogenesis of acne, but also give us more insight (and also much more work to do) with respect to the way the bacteria on our skin can change how skin works at the genetic level.”
The research goes well beyond skin problems, he says, and has “huge implications for microbiome research,” because it highlights how “our many tiny friends who live on our skin have the ability to modify how we work, which has broader implications for other inflammatory diseases.”
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