The National Rosacea Society (NRS) has awarded funding for four new studies as part of its research grants program to advance scientific knowledge of the potential causes and other key aspects of this chronic and potentially life-disruptive disorder that affects an estimated 14 million Americans.
"We are delighted that this important program is resulting in significant new findings toward the further understanding and more effective management of this widespread disorder," said Dr. Jonathan Wilkin, chairman of the NRS medical advisory board, which reviews and selects grant applications for funding. "We are also grateful for the growing thousands of rosacea patients whose donations make this program possible."
Dr. Richard Gallo, chief of the division of dermatology at the University of California - San Diego, and Dr. Kenshi Yamasaki of the Veterans Medical Research Foundation were awarded $25,000 to continue their NRS-funded research of how cathelicidins may play a role in the development of subtype 2 (papulopustular) rosacea.
In previous study results recently published in Nature Medicine, the researchers found that people with subtype 2 rosacea had abnormally high levels of anti-microbial peptides called cathelicidins, as well as an overproduction of anti-inflammatory peptides known as stratum corneum tryptic enzymes (SCTE).1 They also discovered that the high level of SCTE results in a different form of cathelicidin than found in patients without 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 play an important role in the papules (bumps) and pustules (pimples) associated with subtype 2 rosacea.
In the new study, they will examine these and related substances at the molecular level and conduct further tests in animal models. They note that successful results will further support the hypothesis that high levels and an abnormal form of cathelicidin lead to rosacea, opening the way for new therapeutic approaches.
Dr. Yolanda Helfrich, assistant professor of dermatology at the University of Michigan, was awarded $25,000 to compare subtype 1 (erythematotelangiectatic) rosacea and photoaging, both of which may include the development of telangiectasia (visible blood vessels) and erythema (redness). The study will examine the potential differences and similarities of those signs in respective patient groups at a clinical and molecular level, which may increase understanding of the pathogenesis of rosacea as well as lead to improvements in differential diagnosis and treatment.
Dr. Richard Granstein, chairman of dermatology at Cornell University, and colleagues were awarded $25,000 to continue their research on the role of adenosine triphosphate (ATP) in recruiting inflammatory cells in subtype 2 rosacea.
Researchers have found that stress, a common rosacea trigger, may activate the sympathetic nervous system with release of ATP from sympathetic nerves innervating cutaneous blood vessels. Earlier NRS-funded studies had shown that ATP initiates an inflammatory response mediated by human dermal endothelial cells. The researchers will also expand their study to examine whether three other agents produced by nerves elicit effects similar to ATP, and will test whether therapeutic agents for rosacea work by inhibiting the expression of inflammation-causing molecules by endothelial cells.
Dr. Martin Steinhoff, department of dermatology, University of Muenster, Germany, was awarded $25,000 to study the role of neuroimmune interactions in the pathophysiology of rosacea. In an article recently published in the Proceedings of the National Academy of Sciences, Dr. Steinhoff and co-workers revealed a new mechanism by which peptidases regulate the cell signaling of neuropeptide receptors, resulting in the control of neurogenic inflammation. In the new study, by molecular, cellular and genomic approaches, the researchers will attempt to characterize the molecules and receptors involved in the abnormal interaction between neuropeptide receptors and neuropeptidedegrading enzymes, which results in dysregulation and contributes to the development of rosacea.
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.