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JCI table of contents, November 15 2004

avage by exfoliative toxins (ETs) of Staphylococcus aureus, however Amagai et al. found that ETs did not cleave Dsg4, suggesting that Dsg4 could not compensate for the loss of Dsg1 after ET cleavage. In sum, the authors concluded that Dsg4 must play a role other that adhesion in the development of pemphigus and SSSS.

TITLE: Defining the pathogenic involvement of desmoglein 4 in pemphigus and staphylococcal scalded skin syndrome.

AUTHOR CONTACT: Masayuki Amagai
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan.
Phone: 81-3-5363-3425; Fax: 81-3-3351-6880; E-mail: amagai@sc.itc.keio.ac.jp.

View the PDF of this article at: https://www.the-jci.org/press/20480.pdf

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Par1 for the course in inflammatory bowel disease

An estimated more than 1 million Americans suffer from ulcerative colitis or Crohn's disease, the two most common forms of inflammatory bowel disease (IBD), which cause painful and debilitating chronic inflammation of the digestive tract. Thought to result from a variety of genetic and environmental factors, scientists have yet to gain a complete picture of the mechanisms of this disease. In the November 15 issue of the Journal of Clinical Investigation, Nathalie Vergnolle and colleagues found that IBD patients have increased levels of protein-activated receptor1 (PAR1) in the colon. In mice, activation of PAR1 resulted in increased severity and duration of inflammation requiring T and B cells. Conversely, drugs that inhibit PAR1 activity were shown to greatly reduce inflammation. The results point to the importance of PAR1 activity in IBD and indicate that PAR1 inhibition may be useful in treating IBD and other chronic intestinal inflammatory conditions.
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Nov-2004


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