The cells in our skin that fabricate fatty acids could play an unappreciated role in acne breakouts. Recent experiments on human acne and mouse skin have found pimples and lesions are closely regulated by fat-producing fibroblasts.

Fibroblasts are the most common type of connective tissue cell we have in our bodies; they produce and maintain the very structure of our skin, and are critical to wound healing, too. However, their role in acne has been comparatively overlooked.

Researchers have now identified that a subset of skin fibroblasts – these ones are precursors to fat cells – can be triggered by a notorious pimple-forming bacterium called Cutibacterium acnes, responsible for causing the inflammation that characterizes acne.

When confronted with this infection, these particular fibroblasts appear to be stimulated to turn into fat cells in a process called reactive adipogenesis. At the same time, this process also triggers the release of cathelicidin, a peptide with antimicrobial properties.

"These findings may transform the way we treat acne," says dermatologist Richard Gallo from the University of California San Diego.

"Previously, it was thought that hair follicles were most important for acne to develop. In this study, we looked at the cells outside of the hair follicle and found they had a major effect on controlling bacteria and the development of acne."

Acne is the most common skin condition in the United States; over the years, research has unearthed a slew of factors and underlying mechanisms that can lead to it, but there are still some gaps in our understanding that scientists continue to chase.

Much of past research has focused on the hair follicle and its supporting oil gland, which helps to lubricate the pore and clear away dead skin cells or dirt. In those with acne, the follicle can become clogged and certain types of bacteria proliferate within, resulting in inflammation due to the release of toxins and other local effects.

Topical retinoids are useful for the treatment of severe acne, as they can help to 'unclog' pores and reduce inflammation. But they might also help in another way, too.

Skin biopsies on acne patients have revealed that retinoids can enhance the expression of cathelicidin among some skin fibroblasts, while also dampening the growth of more bacteria due to the presence of the newly spawned fat cells. Further tests on mouse models found similar results.

"The influence of fibroblasts on acne development appears to reflect a balance between host and microbe," the authors write.

"Cells stimulated by C. acnes express cathelicidin, which has activity against C. acnes, whereas the induction of increased lipid synthesis appears to promote C. acnes growth."

It's a double-edge sword, but if we can figure out how to dull one side of the immune attack, it could help treat acne more directly.

Today, retinoid treatments are only used in severe cases as they can cause fetal abnormalities if a patient becomes pregnant. If researchers can figure out what triggers the fibroblast to produce cathelicidin, we might be able to give this pimple-fighting peptide an extra boost with fewer side effects.

"Cathelicidin being so highly expressed in acne biopsy tissue was a very interesting finding to us," says Gallo.

"Knowing this will be helpful in developing a more targeted therapy to treat acne."

The study was published in Science Translational Medicine.