So What's Really Building up Inflammatory Bowel Disease?

Monitoring patients' own intestinal immune responses, researchers at Yale University have identified some of the bacterial culprits driving inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis.

Monitoring patients’ own intestinal immune responses, researchers at Yale University have identified some of the bacterial culprits driving inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis.

While the human intestinal microbiota is comprised of trillions of bacteria, the possibility that only a fraction of those bacterial species can potentially severely affect a person’s susceptibility to IBD is quite alarming.

Richard Flavell, PhD, Sterling Professor of Immunobiology at the Yale School of Medicine, said, “A handful of bad bacteria are able to attain access to the immune system and get right at the gut. If you look at the bacteria to which we have made an immune response, you can begin to find these bad actors.”

He and his research team studied the antibody coatings right on the surface of bacteria. “The coating is our body’s attempt to neutralize the bacteria,” Flavell said. “It binds to the bad bacteria.”

According to the journal article, Flavell and his team used “flow-cytometry-based bacterial cell sorting and 16S sequencing to characterize taxa-specific coating of the intestinal microbiota with immunoglobulin A (IgA-SEQ).” This, in turn, suggested increased rates of IgA coating directly identified with colitogenic intestinal bacteria in a corresponding mouse model.

Using the IgA-SEQ coupled with samples of fecal bacteria from the patients themselves, the researchers were able to create personalized gut microbiota culture collections each with predetermined levels of IgA coating. The team found that IgA coating could successfully identify the inflammations causing the disease.

While the team were able to locate the correlation, continued research is underway so the researchers can identify the amount of bacterial species in the intestinal microbiota actually are detrimental. Furthermore, Flavell suggested it prudent to learn whether those bacterial species are common or unique to specific IBD patients. If so, targeted elimination of the bacteria could reduce, reverse, or potentially prevent IBD from further development.

Nevertheless, the study is a step in the right direction, showing the possibility of anti-bacterial therapies like antibiotics, probiotics, or even vaccines.