Medical scientists reported key results of ongoing research on potential causes of rosacea during the eighth annual rosacea research workshop, sponsored by the National Rosacea Society (NRS). The workshop was conducted during the annual meeting of the Society for Investigative Dermatology, and was attended by more than 100 medical researchers from around the world.

"We are very grateful for the growing support of the many thousands of rosacea sufferers who have donated to the NRS research grants program," said Dr. Richard Granstein, head of dermatology at Cornell University, who chaired this year's workshop.

Dr. Granstein presented new findings from his group's broadening investigation of ATP, a neurotransmitter and carrier of chemical energy throughout the body, as participating in an inflammatory pathway in the development of rosacea. In earlier research funded by the NRS, they had found that when ATP is released into the skin by the nerves, a cascade of microscopic events may occur in rosacea patients that likely contributes to the bumps and pimples of subtype 2 (papulopustular) rosacea.¹

Dr. Granstein reported they have now discovered that another neurotransmitter, norepinephrine, may also play a role because it interacts synergistically with ATP to enhance the production of interleukin-6, which leads to inflammation.

Additional researchers have reported new findings related to inflammation as well. "Once we have defined the inflammatory pathways, new medications can be developed that may more effectively block this process," said Dr. Kenshi Yamasaki of the dermatology division at the University of California-San Diego, who along with Dr. Richard Gallo and other colleagues is conducting ongoing research on cathelicidins as a cause of rosacea.

In NRS-funded study results recently published in the scientific journal Nature Medicine, this team of investigators believes they may have identified a key mechanism that could pinpoint the way to a future treatment for the disorder.²

The researchers previously found that small proteins called cathelicidin anti-microbial peptides normally help protect the skin from infection. However, people with rosacea had too much cathelicidin, and it was different from the form seen in people without the disorder. This was due to the overproduction of the stratum corneum tryptic enzymes in patients with rosacea. By putting these two observations together, the researchers were able to induce signs of rosacea in the skin of mice, thus suggesting that these molecules are an important part of causing the disease.

"Rosacea's papules and pustules may actually be the end result of the body's automatic attempt to protect itself gone astray," Dr. Yamasaki said. "As we more fully understand these processes, we may be able to devise new treatments that interrupt them to prevent rosacea's symptoms."

Associated References

1. Seiffert K, Ding W, Wagner JA, Granstein RD. ATPγS enhances the production of inflammatory mediators by a human dermal endothelial cell line via purinergic receptor signaling. Journal of Investigative Dermatology. 2006;126:1017-1027.

2. Yamasaki K, DiNardo A, Bardan A, et al. Increased serine protease activity and cathelicidins promotes skin inflammation in rosacea. Nature Medicine. 2007;13:975-980.