Wed Aug 21, 2002
By Amanda Gardner
WEDNESDAY, Aug. 21 (HealthScoutNews) -- Carbohydrates that are naturally present in the human body may help cause rheumatoid arthritis, a debilitating, painful disease that has no cure and no clear cause.
"Basically, we found that altered recognition and handling of glycosaminoglycans (GAGs) in your body by the immune system can cause rheumatoid arthritis," says Julia Ying Wang, lead author of the new study and an assistant professor of medicine at Brigham and Women's Hospital and Harvard Medical School. "It affects primarily the joints, but also skin and other connective tissues such as tendons."
The findings, which are being presented today at the American Chemical Society's annual meeting in Boston, are in keeping with what is already known about this disease, other experts say.
"Even though it may not be the cause, it may be an important component in the cascade that leads to the damage," says Dr. Mark Jarrett, a rheumatologist and chief medical officer at Staten Island University in New York City. "We certainly feel rheumatoid arthritis is a disease that's immune-mediated. One of the problems is that we've never known what sets off the immune system that promotes the disease. It certainly could be some natural carbohydrates in our body, which, for some reason, are altered or recognized as looking like they're altered by the immune system, and trigger the cascade of inflammation that results in the disease."
GAGs are sugars that are already present in joint cartilage, joint fluid, connective tissue and skin. They do not come from outside the body. "That's why it's called an autoimmune disease. The body attacks itself," Wang explains.
When Wang and her colleagues injected large amounts of GAGs into lab mice, the mice developed symptoms of arthritis, including swelling, inflammation and joint damage.
The same type of GAG-binding cells were also found in tissue taken from people with rheumatoid arthritis. In both mice and humans, the cells which experienced inflammation had receptors that bonded with the GAGs.
Wang suspects rheumatoid arthritis may be initiated by microorganisms either because they present GAGs very similar to our own on their surfaces or because they secrete enzymes that liberate GAGs from the connective tissue.
"This is definitely a very nice target for drugs because we found the same type of cells in humans already," Wang says. "To design inhibitors that block this interaction would be a good drug target."
"It is an important step, even though it may not be the critical step. If you can block that, it certainly might lead to a treatment," Jarrett says.
Drugs developed to attack this mechanism would be classified as biological agents, which target specific parts of the immune system. Biological agents have become more and more important in the treatment of rheumatoid arthritis.
"This complements the work that's ongoing," Jarrett says.