Lots of buzz at the moment about the publicity raised by a nature.com article about Cathelicidins.
Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea
Acne rosacea is an inflammatory skin disease that affects 3% of the US population over 30 years of age and is characterized by erythema, papulopustules and telangiectasia. The etiology of this disorder is unknown, although symptoms are exacerbated by factors that trigger innate immune responses, such as the release of cathelicidin antimicrobial peptides. Here we show that individuals with rosacea express abnormally high levels of cathelicidin in their facial skin and that the proteolytically processed forms of cathelicidin peptides found in rosacea are different from those present in normal individuals. These cathelicidin peptides are a result of a post-translational processing abnormality associated with an increase in stratum corneum tryptic enzyme (SCTE) in the epidermis.
In mice, injection of the cathelicidin peptides found in rosacea, addition of SCTE, and increasing protease activity by targeted deletion of the serine protease inhibitor gene Spink5 each increases inflammation in mouse skin. The role of cathelicidin in enabling SCTE-mediated inflammation is verified in mice with a targeted deletion of Camp, the gene encoding cathelicidin. These findings confirm the role of cathelicidin in skin inflammatory responses and suggest an explanation for the pathogenesis of rosacea by demonstrating that an exacerbated innate immune response can reproduce elements of this disease.
This article is a result of a few years of research by Dr. Gallo. We’ve been reading about this research, some of it sponsored by the NRS, since at least the Fall of 2002.
The upside of this is that rosacea is getting publicity that it sorely needs. Nature is a very prestigious journal, so this publicity is excellent and will encourage Dr. Gallo and his colleagues to keep going.
The downside is that some of the follow up articles in the newspapers are overstated and give a false impression of the immediate implication of the research. There isn’t any new treatments just around the corner as a result of this research, and the cause/cure didn’t suddenly get hugely closer.
What is has shown, though, is that the inflammatory pathway that causes most rosacea symptoms is key to making good progress. While cathlecidins may be a key product of inflammation I’d be much more excited about seeing research that found the starting point of the inflammatory pathway. Blocking the inflammation at the source will always be more effective than trying to treat the downstream toxins.
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just wanted to clarify. You mentioned “..cathlecidins may be a key product of inflammation..”.
The article is actually saying that cathlecidins are involved in causing the inflammatory response. In rosacea, the cathlecidins are overproduced and processed differently than in non-sufferers, resulting in an exagerated downstream inflammatory response.
a normal response to bacteria, but are overproduced and
Sorry, please ignore “a normal response to bacteria, but are overproduced and”