For those studying inflammation, the name of the game has been initiation. How does the immune system initiate the inflammatory process? And, more to the point therapeutically, is it possible to develop treatments that intervene in the process for those with chronic inflammatory conditions such as arthritis and periodontal disease? In recent years, however, the game plan has expanded considerably with the discovery that inflammation is “self-limiting.” Or, in more lay terms, like logging off a computer, the process also involves circuitry that naturally shuts down and resolves the inflammation. Among the signals passed along this anti-inflammatory circuitry are those mediated by a group of compounds called resolvins. In the Journal of Biological Chemistry (August 11), National Institute of Dental and Craniofacial Research (NIDCR) grantees and colleagues add a new layer of detail into how specifically the resolvin called RvE1 is inactivated. The researchers also report developing a stable analog of RvE1 that was as potent as the natural compound in reducing the infiltration of immune cells that are known to be present in uncontrolled inflammation. The authors noted that the RvE1 analog will be a useful tool in further dissecting the resolution process and, hopefully, designing targeted treatments to help people with disorders of aberrant inflammation
(Source: NIDCR, Science News in Brief, Sep 8, 2006)
