Prevention by Prediction: Gut Bacteria and Rheumatoid Arthritis

Benjamin Franklin said, “An ounce of prevention is worth a pound of cure.” Going even further with that idiom, being able to predict an illness would certainly help in preventing it. As highlighted in a Daily Dose results from a study suggested that the presence of certain types of gut bacteria might indicate susceptibility to rheumatoid arthritis (RA). Lead author of the study, Veena Taneja, PhD, is an Immunologist at Mayo Clinic in Rochester, Minnesota.

Q. What steered you and your team to this research?

A. Genetic factors have been associated with predisposition to rheumatoid arthritis (RA). However, since not all patients have the RA-associated genes, environmental factors like smoking and infections are also known to be involved. Our gut harbors trillions of bacteria. So the thought that an opportunistic commensal in certain conditions could cause inflammation is not surprising. The gut is the largest organ that is exposed to environmental factors daily, and the gut microbiota is influenced by those environmental factors. We set out to determine if any commensal(s) are expanded in RA patients but not present in healthy individuals. Also, we were interested in finding out if we can use beneficial commensals that have reduced inflammation in some patients as well as suppressed inflammation in others. Our thought was that using endogenous commensals for treatment will have none of the side effects that are observed with current drugs.

Q. Do you plan to study a larger group of people?

A. We are validating our observations with a larger group of patients and also trying to determine if we can use the gut microbiota as predictor for RA and drug response.

Q. How did you recruit your patients?

A. Patients attending the rheumatology clinic at Mayo clinic and those who were diagnosed to have RA by the set criteria were approached and asked if they would like to enroll for the study. Those patients who agreed were recruited.

Q. How do you get the gut microbial?

A. We used stool samples to get a window in to the gut microbiota.

Q. What is the next step in your research?

A. I would like to perform some basic research to determine the mechanism by which gut microbes cause inflammation or suppress inflammation. This will help in determining the pathways that can be targeted for therapies.

Q. What sort of preventative treatments might be developed?

A. There are a couple of ways this can be approached. One way is to use a commensal that can be beneficial for RA and other inflammatory diseases and secondly, it can be a path toward personalized medicine in which patients can be given the beneficial microbes they are lacking. The other approach for preventative treatment could be to use the gut microbiota as predictor especially in families where RA and other autoimmune diseases are present so individuals who are at risk can be identified and treated accordingly.

Q. Your second study was in arthritis susceptible mice. Are humans the next step?

A. I hope we can apply the information we gained in the mice study to humans for the benefit of patients.

Q. Is the hope that this test will be a standard one in practitioner’s armamentarium?

A. My hope is that we can devise a test that will help a practitioner to diagnose the problem earlier as well as treat patients in an individualized way as a standard practice.

Q. Will this treatment be expensive?

A. The technology to sequence gut microbiota is relatively new and therefore costly, but with time it is becoming cheaper. At present I don’t know when and how the treatment will be available in the clinic so I cannot comment on this.

Q. When you’re not working, how do you like to spend your free time?

A. I like to read fiction and nonfiction.

Q. What is a dream project you hope to work on?

A. I would like to perform a clinical trial with the commensal we have identified for treating patients. I would like to perform a study to determine the mechanism by which this commensal changes the immune response and suppresses inflammation.

We thank Veena Taneja, PhD, for her time.


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