In major newspapers across the country they are saying scientists have found the
cause of
rosacea. For instance the Los Angeles Times, the Washington Post, and Medical
News
Today.
Here are the links >
http://tinyurl.com/yp9xjg
http://tinyurl.com/2eglqn
http://tinyurl.com/2ncnuc

Here is the Abstract
Increased serine protease activity and cathelicidin promotes skin inflammation
in rosacea
Kenshi Yamasaki, Anna Di Nardo, Antonella Bardan, Masamoto Murakami, Takaaki
Ohtake,
Alvin Coda1, Robert A Dorschner1, Chrystelle Bonnart, Pascal Descargues, Alain
Hovnanian, Vera B Morhenn & Richard L Gallo
Nature Medicine, 5 August 2007 | doi:10.1038/nm1616; http://www.nature.com [type
in
rosacea in the search box]

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
telangiectasia1, 2, 3.
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
peptides4. 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.


1. Division of Dermatology, University of California, San Diego, and VA San
Diego Health
Care System, 3350 2. La Jolla Village Drive, San Diego, California 92161, USA.
3. Department of Dermatology, Asahikawa Medical College, Asahikawa 078-8510,
Japan.
4. Department of Medicine, Asahikawa Medical College, 2-1-1-1 Midorigacka
Hidashi,
Asahikawa 078-8510, Japan.
5. INSERM, U563, Toulouse F-31000, France.
Université Paul-Sabatier, Toulouse F-31000, France.
6. CHU Toulouse, Department of Genetics, Place du Dr. Baylac, Toulouse F-31000,
France.