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DNA Sequencing Tests Whether Intestinal and Oral Bacteria Trigger RA


 

FROM THE ANNUAL MEETING OF THE AMERICAN COLLEGE OF RHEUMATOLOGY

ATLANTA – Preliminary data suggest naturally occurring bacteria in the mouth and intestine might trigger the inflammation that causes rheumatoid arthritis, according to findings presented in a press conference at the annual meeting of the American College of Rheumatology on Nov. 8.

"We are testing an old hypothesis with new technology," said Dr. Jose Scher of New York University. The ongoing study is the first to use DNA technology to bypass the cumbersome bacterial culture process. Dr. Scher and his colleagues used DNA sequencing to identify all the bacteria present in the mouths and intestines of study participants. This technology finally allows researchers to explore a long-standing theory that oral and intestinal bacteria might trigger rheumatoid arthritis (RA) by activating Th17 cells.

To date, 90 patients have been enrolled in the study, including 55 adults with RA and 45 healthy controls, Dr. Scher said in an interview. Of these, 22 RA patients and 14 controls have undergone DNA sequencing.

When the researchers examined oral microbiota, patients with early-onset RA had three to four times more Porphyromonas gingivalis bacteria (implicated in gum disease) than did healthy controls. In general, gum disease is present in approximately 82% of chronic RA patients and 75% of new-onset RA patients, Dr. Scher noted.

In addition, intestinal bacteria associated with inflammation were more prevalent in RA patients, compared with controls. The Prevotellaceae species of bacteria was identified in approximately 80% of the RA patients, compared with the 20% usually found in healthy individuals, he said.

The results are preliminary, but the findings support data from previous studies showing a high prevalence of oral disease in RA patients, said Dr. Scher. The study is ongoing, and the next steps for research include using antibiotics to modify the microflora in the body and identify how the bacteria cause inflammation, he added, noting that, ideally, researchers would then develop strategies to reduce or prevent the inflammation before it caused RA.

The study was supported in part by funding from the National Institutes of Health. Dr. Scher said he had no financial conflicts to disclose.

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