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Protein Helps Spur Rheumatoid Arthritis

The finding might lead to new drugs against the crippling disease

FRIDAY, Dec. 2, 2005 (HealthDay News) -- Adding another piece to the rheumatoid arthritis puzzle, a team of British researchers believe they've discovered the role a key protein plays in the painful inflammatory joint condition.

The protein, Type II Collagen (CII), appears to be modified at the onset of rheumatoid arthritis (RA). It then morphs into a destructive anti-immunity weapon that weakens the body's immune system while promoting the chronic inflammation of joints.

The finding might someday point to new drug targets against the disease, the scientists said.

"Our study has important implications for the further study and enhanced understanding of the pathology of RA," said study author Ahuva Nissim, of the Queen Mary's School of Medicine and Dentistry at the University of London.

A chronic, painful and often disabling autoimmune disease that affects more than 2 million Americans, rheumatoid arthritis is defined by severe inflammation of the lining of the joints. This inflammation leads to a slow degeneration of bone and cartilage over time. According to the Arthritis Foundation, women are two to three times more likely to be stricken with the illness then men.

Nissim's team set out to better understand the disease, which to date has no clear cause and no known cure.

To do so, they honed in on RA's effect on Type II Collagen (CII) -- a major protein component of cartilage, bone and tendons.

The team theorized that CII -- normally a key player in healthy joint function -- might also help spur RA when stressed by inflammation.

They noted that when inflammatory cells enter joint tissue they over-consume oxygen. In turn, oxygen depletion undercuts the function of otherwise healthy proteins by modifying them in such a way as to encourage binding with sugar molecules.

This binding further encourages inflammation. The result: a vicious biochemical cycle that results in chronic RA pain.

To determine whether CCII was, in fact, one of the principle culprits in this process, the researchers first obtained blood serum samples from 31 male and female RA patients between the ages of 65 and 93.

Blood specimens were also taken from 41 patients suffering from other inflammatory joint diseases, such as back pain, osteoporosis and gout.

All the samples were exposed to normal CII protein taken from cows, as well as CII modified with one of three oxidants or a common sugar -- all of which are present during the inflammation typically found in a rheumatic joint.

Reporting in the December issue of Arthritis and Rheumatism, the authors say the normal form of the CII protein rarely bound with antibodies from blood samples taken from RA patients.

However, 45 percent of the RA blood samples showed evidence of antibody binding when exposed to the altered form of the protein. In fact, the binding rate was four times higher than that seen with non-modified CII.

Modified CII did not bind as often with blood drawn from non-RA patients , they added.

Based on these findings, the researchers believe RA alters CII proteins to further upset the immune response and perpetuate the disease.

According to the researchers, these early results could lead to practical treatment benefits, both through new clinical insights into how RA works and by highlighting novel targets for intervention.

"In the future, understanding of this process will help us develop specific therapeutics which will target only the inflamed joints," Nissim said.

Others expressed doubt the findings will have that great of an impact, however.

"It's nothing that blows your socks off," commented Dr. Stephen Lindsey, head of rheumatology at Ochsner Clinic Foundation Hospital in Baton Rouge, La.

"It's is a promising avenue of research in trying to develop further what's making RA such a chronic disease," he added. "They're looking at why the body forms immunological reactions against itself, which it's not supposed to do. But I think it's interesting, more than it is leading to any promise of new therapies."

More information

For more on rheumatoid arthritis, check out the Arthritis Foundation.

SOURCES: Ahuva Nissim, Ph.D., Queen Mary's School of Medicine and Dentistry, University of London; Steven Lindsey, M.D., head, rheumatology, Ochsner Clinic Foundation Hospital, Baton Rouge, La.; December 2005 Arthritis and Rheumatism
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