Researchers at the Massachusetts Eye and Ear Infirmary ( MEEI ) have found that Chlamydia pneumoniae, a bacterium linked to heart disease and capable of causing chronic inflammation, was present in the diseased eye tissue of five out of nine people with neovascular, or "wet," age-related macular degeneration ( AMD ).
However, it was not found in the eyes of more than 20 individuals without age-related macular degeneration, providing more evidence that this disease may be caused by inflammation.

The study is published in the Archive for Clinical and Experimental Ophthalmology.

Age-related macular degeneration is the leading cause of blindness in Americans over the age of 55. The majority of vision loss is due to neovascular age-related macular degeneration, the advanced form of the disease characterized by the formation of blood vessels in the macula, the center part of the eye's retina. These blood vessels often leak, thus giving neovascular age-related macular degeneration the name of "wet" AMD.

Researchers at the MEEI and Harvard Medical School ( HMS ) examined nine wet age-related macular degeneration membranes for the presence of C. pneumoniae and also determined whether this pathogen can change the function of eye cells in ways that can cause wet age-related macular degeneration.

They found C. pneumoniae in the eyes of five out of the nine patients with wet age-related macular degeneration. They also tested tissue from more than 20 people who did not have age-related macular degeneration and did not find C. pneumoniae in any of these normal eye tissues.

" The paper showed that C. pneumoniae is capable of modifying the function of important cell types involved in regulating normal eye function," said lead author Murat Kalayoglu. " We found that C. pneumoniae infection led to increased production of vascular endothelial growth factor ( VEGF ), the key protein involved in wet age-related macular degeneration.
That C. pneumoniae infection of human eye cell types increases VEGF production is therefore significant and could explain in part why VEGF levels are increased in many people with wet age-related macular degeneration."

Most of the new medications to treat wet age-related macular degeneration, such as Macugen and Lucentis block VEGF.

The study comes at a time of great interest in inflammatory mediators of age-related macular degeneration.
Over the past seven months, a flurry of high-impact papers have shown, in aggregate, that nearly 50 percent of age-related macular degeneration 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 age-related macular degeneration," 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 age-related macular degeneration 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 age-related macular degeneration 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 age-related macular degeneration," he said.

" This is an important study suggesting that infection with C. pneumoniae may be a critical link between a genetic predisposition to age-related macular degeneration and actual progression to disease," said Gerald I. Byrne, 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 ulcers. Those studies were viewed with skepticism, but Marshal and Warren, the researchers who pioneered that work received the Nobel Prize this year."

Source: Harvard Medical School, 2005


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