New research pinpoints the genes associated with rheumatoid arthritis joint damage and shows just how exercise can block inflammation.
Two new studies presented at the European League Against Rheumatism’s annual conference are shedding light on rheumatoid arthritis (RA) symptoms and severity.
The first indicates that exercise can briefly suppress local and whole-body inflammation. This is important because ongoing inflammation, swelling, and pain in the joints are common symptoms of more than 200 rheumatic diseases. Over time, that chronic inflammation can damage the affected joints.
Nicholas Young, Ph.D., a study author from Ohio State University’s Wexner Medical Center, said his research is focused on the physiological changes that occur as a result of working out. Physical activity generates a biological response and brings about changes on a molecular level.
Young’s research team studied the NF-kB protein, which is active in many inflammatory diseases. They conducted experiments on mice, some of which received no treatment, some of which only exercised, and some of which were given an injection of lipopolysaccharides (LPS). A fourth group of mice exercised for seven days before receiving an LPS injection, and a fifth group worked out after the injection.
The scientists found a strong local and whole-body inflammatory response when they injected LPS, with the response strongest two hours after the injection. NF-kB was detected in lymphatic tissues throughout mice’s bodies, but in the groups that exercised before and after the injection, NF-kB was not nearly so active. Exercise blocked NF-kB, but only for about 24 hours.
Exercise, by inhibiting NF-kB, was able to suppress many pro-inflammatory cytokines. Cytokines are proteins that play an important role in cell signaling.
“As the inflammatory process in rheumatic diseases is a major cause of disability, we are excited to uncover the process by which exercise works on a molecular level to decrease this inflammation. Our results show the benefits that exercise could have in decreasing the great burden of rheumatic diseases. They also highlight the need for frequent exercise in order to create clinically significant results,” Young said in a press release.
Dr. Paul Sufka, a rheumatologist from Minnesota, said that patients are always looking for natural treatments to reduce inflammation.
“It is extremely promising to hear that inflammation appears to be reduced by exercise,” he said. “Unfortunately, many of our patients with inflammation suffer from pain that complicates exercise, so hopefully this will lead to further research looking into what types, intensity, and duration of exercise are sufficient for an anti-inflammatory response.
Another study presented at the conference pinpointed genetic markers linked to RA outcomes and treatment responses. Researchers looking at data from three independent studies found that the amino acid valine at position 11 on the HLA-DRB1 gene is the strongest independent genetic predictor of joint damage in RA patients. Positions 71 and 74 were also found to be predictors. All three positions together—11, 71, and 74—were strongly linked to joint damage and early death.
However, the HLA-DRB1 gene variations linked to RA susceptibility and severe outcomes also told researchers which patients would likely have a positive response to anti-TNF drug treatment.
“This major advance in genetics might allow stratification of RA patients at the onset of their disease to identify those at risk of joint damage and early death, and also those who are more likely to respond to anti-TNF biological therapy,” said Dr. Sebastien Viatte of the Arthritis Research U.K. Centre for Genetics and Genomics at the University of Manchester in a press release.