What Really Causes Pimples?

Acne is one of the most common, chronic skin diseases, affecting more than 85 percent of teenagers and adults at some point.
How a pimple pops up has been a controversial question for years, as there are multiple factors at play, including excess oil/sebum production from the sebaceous glands, abnormal growth of the skin lining the hair follicle, inflammation, and bacterial colonization of the hair/sebaceous gland unit by the bacterium Proprionibacterium acnes.
For years, the concept of non-inflammatory and inflammatory acne has dominated our treatment approach. Noninflammatory acne means whiteheads and blackheads, while inflammatory acne means small to large red and pus-filled pimples. But more recently, we’ve learned that in fact ALL acne is inflammatory – even if you can’t see it on the skin, immune cells surround the hair follicle well before any sign of acne is visible to the naked eye.
A significant amount of research in the past 10 to 15 years has shown how part of the immune system, called the innate immune system (the first responder that signals the alarm if there are any infectious invaders), reacts inappropriately to P. acnes and calls in the immune troops. Elements of this immune system (called Toll-like receptors and inflammasomes) orchestrate the process, and it is therefore no surprise to dermatologists that while some of our current treatments work, they also inhibit these alarm systems.

Oil Glands That Do More Than Produce Oil

So where does the oil gland fit in to all this? Well, that bacterium P. acnes certainly enjoys the delicacy that is our sebum and can convert it into fatty acids (instead of fats), which can stimulate inflammation. But is that all? It seems the answer is NO. In a recent paper in the Journal of Investigative Dermatology, scientists found that cells making up skin oil glands do more then just make oil – they actually function as part of the immune system. Sebaceous gland cells that secrete sebum/oil express an inflammasome recently shown to be central to the inflammation that results in acne. Now there is probably good reason for this – the inflammasome is there to protect us from infectious agents just dying to get into our skin. However, with acne, it turns out too much of a good thing is a bad thing.
This research is important for several reasons. First, it further explains the role of sebaceous gland cells in the development of acne (they don’t just produce sebum!). More exciting though, by understanding the mechanisms of immune activation in sebaceous glands, we could find new approaches to the prevention and treatment of acne. Stay tuned!