- Researchers investigated the effects of acne-related bacteria, C. acnes, on skin barrier health.
- They found that C. acnes increases skin lipid production and boosts the skin’s barrier function, keeping it lubricated and increasing antimicrobial activity.
- The findings could lead to novel treatments for acne and other skin conditions.
The skin is the human body’s largest organ. It has multiple
Lipids are essential to the skin’s function. Disturbances to these lipids can lead to skin conditions such as
Cutibacterium acnes (C. acnes) is one of the
Understanding more about how C. acnes influences lipid synthesis on the skin could help researchers develop new treatments for acne and improve skin barrier health.
Recently, researchers found that C. acnes helps balance the skin’s microbiome, reduce water loss from the skin, and increase its resistance to microbial invasion.
Dr. Christopher Bunick, an associate professor of dermatology at Yale School of Medicine, who was not involved in the study, told Medical News Today:
“There is a misconception surrounding acne vulgaris that all lipids, fats, or oils on human skin are bad and make acne worse. This misconception extends to C. acnes, where this bacterium is blamed for acne but not credited for the healthy benefits it provides human skin.”
“Here, we learn that C. acnes produces compounds that stimulate human skin to produce helpful lipids that keep our skin soft, moist, and functioning as a barrier. This work adds to the growing body of literature showing that the human microbiome can act as true symbionts, providing key health advantages to their human host.”
— Dr. Christopher Bunick
The study was published in Microbiology.
For the study, the researchers exposed human skin keratinocytes—cells that make up the skin’s top layer known as the epidermis—to various kinds of bacteria found on human skin.
Among all of the bacteria tested, C. acnes alone triggered an increase in lipid production among skin cells. In particular, it increased lipid levels by three times, including cholesterol, free fatty acids, and triglycerides. Each of these fats plays a key role in protecting the skin barrier.
From further tests, the researchers found that the lipid increases were primarily driven by the production of a short-chain fatty acid called propionic acid, which creates an acidic skin environment. Among multiple benefits, it is known to limit pathogen growth, reduce Staphylococcus infections, and contribute to anti-inflammatory effects in the gut.
The researchers next sought to see how C. acnes increases propionic acid production. Through a series of genetic tests, they found that the acid increases lipid production via a PPAR-alpha signaling pathway. PPAR-alpha is a hormone receptor that regulates the oxidation and transport of fatty acids.
Stimulating ceramide production
By stimulating the PPAR-alpha pathway, C. acnes is able to increase lipid synthesis in skin cells—particularly of triacylglycerols, a major dietary lipid found in plants and animal fats. The researchers noted that these triacylglycerols then break down into fatty acids that serve as precursors to ceramides, lipids that play a crucial role in skin barrier health.
“[The researchers ultimately showed] that C. acnes-induced lipid accumulation in skin cells directly improves skin barrier function, such as by reducing water loss and increasing antimicrobial activity,” said Dr. Bunick.
Dr. Bunick said it may be tempting to think that the study explains how acne develops. However, rather than ‘solve the riddle’ of why humans get acne, he said the study speaks to how skin bacteria like C. acnes contribute to skin health by stimulating lipid production from keratinocytes.
“The authors showed that some of these lipids can have antimicrobial effects, thereby protecting human skin from infection from undesirable bacteria,” he explained.
“However, they note a limitation of their study was they did not identify which C. acnes-induced lipids specifically have antimicrobial function. What this study does do is raise more questions about the role of lipid dysregulation in acne pathogenesis,” he added.
MNT also spoke with Dr. J. Wes Ulm, a bioinformatic scientific resource analyst and biomedical data specialist at the National Institutes of Health, who was not involved in the study.
He noted that the findings are limited as the researchers used human skin samples and mice’s top skin layer, “which may or may not fully translate to findings in actual patients.”
Dr. Bunick said that the findings suggest that stimulating the PPAR-alpha pathway via propionic acid or similar compounds might improve the human skin barrier and thus reduce acne.
“What is more intriguing to me is the entire role of the PPAR receptor family in acne pathogenesis,” he said.
“While [authors of the study] show the importance of PPAR-alpha in lipid barrier regulation, other researchers, like Dr. Mauro Picardo from Italy, already have a PPAR-gamma modulator in clinical trials that has demonstrated substantial acne reduction,” he continued.
“Understanding the differential roles of PPAR alpha and gamma on the pilosebaceous unit—the hair follicle area—where acne occurs, seems of paramount importance [given both findings],” he concluded.