“This is a marker that’s useful in helping predict who will go on to develop RA.”

The University of Colorado School of Medicine has uncovered the shocking finding that people who are genetically inclined to develop the inflammatory disease rheumatoid arthritis (RA) may be affected by specific types of bacteria found in the human digestive tract.

Serologic markers can be used to identify patients at risk for Rheumatoid Arthritis (RA), and these markers can be present in the blood for many years before diagnosis, as was demonstrated by new work led by co-authors Drs. Kevin Deane, Kristen Demoruelle, and Mike Holers here at CU.

One of the antibodies they examined belongs to the type of antibodies we typically see in circulation, whereas the other is an antibody we typically connect with our mucosa, whether it be the mucosa of the mouth, the stomach, or the lungs.

The authors “started to wonder, ‘Could there be something at a mucosal barrier site that could be driving RA?'”

With help from a group at Stanford University led by Bill Robinson, MD, PhD, the researchers at CU took the antibodies made by immune cells from people whose blood markers showed they were at risk for the disease and mixed them with the feces of the people at risk to find the bacteria that the antibodies had marked.

The newly discovered bacteria were then housed in animal models to further test the researchers’ hypotheses. These tests revealed that the bacteria not only caused the animal models to develop the blood markers observed in people who are at risk for RA but that some of the animals also developed full-blown RA.

They found that “the 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,” adds Kuhn. 

“Through studies in human and animal models, we were able to identify these bacteria as being associated with the risk for developing RA. They trigger an RA-like disease in the animal models, and in humans, we can show that this bacterium seems to be triggering immune responses specific to RA.”

According to Kuhn, it may be possible to use medication to target specific species of bacteria in order to stop the immune response from occurring in people who are already at risk for developing RA.

The next step, according to Kuhn, is to determine whether these bacteria are associated with other genetic, environmental, and mucosal immune responses as well as the eventual development of RA in larger populations of people at risk for the disease.

“Then we could say, ‘This is a marker that’s useful in helping predict who will go on to develop RA,’ and apply prevention strategies. The other opportunity there is that if we can understand how it is triggering these immune responses, we might be able to block the bacteria’s ability to do that. “

According to Kuhn, it took five years to conduct and analyze the research, which was ramped up by volunteers who learned they were at risk for RA. The ultimate goal of the research is to determine the precise mechanism by which the bacteria initiates the immune response as well as potential mitigation strategies.

There are numerous new technologies that, according to her, could target particular bacteria in the gut microbiome in order to stop them from having immunogenic effects on the host. “Antibiotics have been considered as a potential treatment for RA for a very long time, but instead of the sledgehammer effect of a standard antibiotic that will wipe out a huge group of bacteria, we might be able to selectively target this bacterium or its effects,” the researcher adds.

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