Adult tick, SEM generated (image courtesy of the International Scientific Working Group).

According to the Centers for Disease Control, more than 20,000 people contracted Lyme disease in 2003. Typically, about 60 percent of people afflicted also develop a painful form of arthritis. One University of Missouri College of Veterinary Medicine researcher is trying to determine how this type of arthritis develops in an effort to identify causes of arthritis and how to prevent it.

"While most people affected with Lyme disease do develop arthritis, some do not and we're attempting to identify the differences between the two," said Dr. Charlie Brown, an assistant professor of veterinary pathobiology. "These different degrees of resistance happen in almost every disease. We need to determine the specific mechanisms the body uses to fight the infection and learn how these might be different when arthritis develops and when it doesn't."

When the body is first infected with Borrelia burgdorferi, the agent of Lyme Disease, blood cells called neutrophils are the body's first response to the infection. Neutrophils are recruited to the site of infection in large numbers and die in large numbers. They are summoned to the infection site by a process involving the release of chemical messengers called chemokines. The chemokines act as a type of telecommunication, informing the neutrophils of the infection and telling them where to go. However, in this particular response, the immune system creates a large amount of collateral damage. In an effort to fight the infection, healthy tissue is damaged at the same time in the joint areas of the body where the infection has grown, eventually causing arthritis.

In Dr. Brown's research was published in The Journal of Immunology and the journal Infection and Immunity. In his articles he said that he found that the infected joints did not develop arthritis when neutrophils did not respond to the infection. However, Dr. Brown also found that mice that were infected, but did not have neutrophils attacking the infection, did not experience an increase in Lyme disease bacteria.

"The next step is to determine what cells are making the chemokines responsible for alerting neutrophils about the Lyme disease infection," Dr. Brown said. "If we can stop the neutrophils from getting to the site of the infection, we might be able to stop the arthritis from forming. This line of research might identify new therapeutic targets and could have implications for other arthritis-related research as well."

The research was funded with grants from the National Institutes of Health for about $1 million.

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