One moment bacteria on the skin are harmless, the next they are causing a full-on spotty break out. Now researchers have discovered exactly why this happens – a breakthrough that could yield new acne treatments, possibly in two years.
Richard Gallo of the University of California, San Diego, and his colleagues have discovered that a harmless bacterium that lives on the surface of the skin can turn nasty, triggering inflammation and zits, when it finds itself trapped in airless, oily conditions like those found in hair follicles.
Cascade of chemicals
The airless environment causes the bacterium, Propionibacterium acnes, to turn sebum – an oily matter found in the skin – into fatty acids that activate inflammation in nearby skin cells. By analysing mixtures of the bacteria alongside human skin and hair cells, Gallo’s team found that the fatty acids deactivate enzymes called histone deacetylases that normally act as a brake on inflammation. Once that brake is off, cascades of chemicals are produced by skin cells, aggravating the type of inflammation that causes acne.
“For the first time, it shows how fatty acids derived from P. acnes act on skin cells to induce inflammation,” says Holger Brüggemann of Aarhus University in Denmark, who in 2004 unravelled the entire genome of the skin bacterium.
Unfortunately, scrubbing your face isn’t the answer, because the bacteria clump together to form structures called biofilms, which help anchor them to the skin. Potential therapies are further complicated by the fact that certain strains of P. acnes are actually beneficial to skin health. Nevertheless, Gallo is confident that his team’s breakthrough could lead to new treatments. “We can either inhibit these fatty acids, or block their impact on the skin,” says Gallo. “We’re working on how to do this.”
Gallo says the discovery could also help to explain why some people seem more prone than others to developing acne. It could be that some people’s hair follicles are especially suffocating. Alternatively, some people might inherit genes that make their skin cells more vulnerable to inflammation from the fatty acids produced by P. acnes, or they may have strains of the bacteria on their skin that make excessive amounts of the fatty acids. “I think all of these aspects probably play a role,” he says.
Brüggemann says that teenagers are most vulnerable to outbreaks because surges in sex hormones during puberty drive the production of extra sebum in the skin. This extra sebum enables any P. acnes in the hair follicles to produce more of the fatty acids that aggravate inflammation, leading to more spots.
Gallo wants to do further work on skin samples to corroborate the findings. “If we get lucky, it could lead to new medications in two to five years,” he says.
Journal reference: Science Immunology, DOI: 10.1126/sciimmunol.aah4609