Researchers at the University of Colorado School of Medicine, in the US, have discovered that some gut bacteria may be responsible for triggering rheumatoid arthritis (RA) in people already at risk of developing the autoimmune disease.

Dr. Kristine Kuhn led a team of researchers from the Division of Rheumatology in a study published Oct. 26 in the journal Science Translational Medicine. Student Meagan Chriswell is the lead author of the paper.

“Work led by co-authors Dr. Kevin Deane, Dr. Kristen Demoruelle, and Dr. Mike Holers here at CU has helped establish that we can identify people at risk for RA based on serological markers and that these markers can be present in blood with many years before diagnosis,” says Kuhn.

“One of these antibodies is part of the normal class of antibodies that we normally see in circulation, but the other is an antibody that we typically associate with mucosa, whether it’s the oral mucosa, the intestinal mucosa, or the lung mucosa. We started to wonder, ‘Could there be something about a mucosal barrier that could lead to RA?'” she continued.

How is rheumatoid arthritis triggered by some gut bacteria?

The CU researchers, with the help of a group led by Dr. Bill Robinson of Stanford University, also in the US, took antibodies made by immune cells from individuals whose blood markers showed they were at risk of the disease and -they mixed it with the feces of people at risk to find the bacteria that are targeted by the antibodies.

To further test their hypothesis, the researchers used animal models to harbor the newly discovered bacteria. These experiments showed that the bacteria not only caused the animal models to develop the blood markers found in people at risk for RA, but some of the models showed full development of RA.

“Our collaborators led by Dr. Eddie James and Dr. Jane Buckner of the Benaroya Research Institute confirmed that T cells in the blood of people with RA will respond to these bacteria, but people who are otherwise healthy do not respond to these bacteria,” says Kuhn.

“Through studies in humans and animal models, we have been able to identify some gut bacteria as being associated with the risk of developing RA. They trigger a disease similar to rheumatoid arthritis in animal models, and in humans, we can show that this bacterium appears to trigger immune responses specific to RA,” the researcher continued.

This study could lead to finding a better treatment

If the unique species of bacteria is indeed driving the immune response that leads to RA in individuals already at risk for the disease, Kuhn says, it may be possible to target the bacteria with drugs to prevent that response.

“The next thing we want to do is identify, in larger populations of individuals at risk for rheumatoid arthritis, whether these bacteria correlate with other genetic, environmental, and mucosal immune responses, and then ultimately with PR development,” says Kuhn.

“Then we will be able to say, ‘This is a marker that is useful to help predict people who will develop RA,’ ​​and apply prevention strategies.” The other opportunity is that if we can understand how these immune responses are triggered, we could block the bacteria’s ability to do that,” she explained.

A new treatment could eliminate the need for antibiotics

The research took five years, Kuhn says, which was helped by people who discovered they were at risk for RA and volunteered to support the study. Ultimately, the researchers want to examine exactly how the bacteria trigger the immune response, as well as different methods of preventing the reaction, they report Medical Xpress.

“There are a lot of different technologies that are just starting to emerge that could selectively target specific gut bacteria, for example, to prevent immunogenic effects on the host,” she says.

“For a long time, people have thought that antibiotics might be a useful therapy for RA, but rather than the sledgehammer effect of a traditional antibiotic that will kill a large group of bacteria, we could selectively target that bacteria or its effects “, concluded the researcher.

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