The study comes at a time of great interest in inflammatory mediators of AMD. Over the past seven months, a flurry of high-impact papers have shown, in aggregate, that nearly 50 percent of AMD can be explained by variations in a gene called Complement Factor H (CFH). This gene makes a protein that regulates the immune and inflammatory responses of the body.

"Our hypothesis is that C. pneumoniae may be the key link between CFH and AMD," Kalayoglu said. "That is, patients with CFH variations may be particularly susceptible to the damaging effects of chronic infection, and an infectious organism like C. pneumoniae may be particularly effective in accelerating inflammation and driving progression of AMD in these patients."

Kalayoglu and colleagues are currently collaborating with CFH researchers to study this hypothesis. "It may be possible to stop or reverse progression of AMD by identifying susceptible patients by diagnostic testing, and then treating these susceptible patients. Although C. pneumoniae is a bacterium that might respond to some antibiotics, much more work needs to be done before considering antibiotic therapy for AMD," he said.

"This is an important study suggesting that infection with C. pneumoniae may be a critical link between a genetic predisposition to AMD and actual progression to disease," said Gerald I. Byrne, Ph.D., professor and chairman of the Department of Molecular Sciences University of Tennessee Health Sciences Center. "This is yet another example of how an infection may unexpectedly contribute to a chronic disease. Certainly the association of C. pneumoniae with heart disease sets the stage for this pathogen's involvement in other chronic conditions. This work is, in some ways, reminiscent of studies done more than 15 years ago on infections and
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Contact: Mary E. Leach
mary_leach@meei.harvard.edu
617-573-4170
Harvard Medical School
7-Nov-2005