Celiac disease–the inability to tolerate food containing gluten–has long puzzled scientists. The puzzle may have finally been solved.
Researchers at McMasters University found that even when people have a genetic predisposition to developing celiac disease, it’s the presence of a particular kind of gut bacteria that acts as a trigger.
Celiac disease is an autoimmune disorder in which the protein gluten–found in grains like wheat, rye and barley–causes the body to attack the small intestine. The autoimmune response damages the villi. These are small finger-like projections in the small intestines that are responsible for absorbing nutrients.
Although celiac disease is hereditary, not everyone with the potential actually develops the disease and researchers have wondered why.
“Celiac disease is caused by gluten in genetically predisposed people, but bacteria in our gut could tip the balance in some people between developing the disease or staying healthy,” senior author Elena Verdu, MD, PhD, said in a press release.
Dr. Verdu is an associate professor of medicine for the Michael G. DeGroote School of Medicine at McMasters University.
According to Dr. Verdu and colleagues, approximately 40 percent of the population have the genetic potential for celiac disease. Only one percent, however, actually develop the disease when exposed to gluten.
The researchers treated mice with two different gut bacteria. One group received Pseudomonas aeruginosa (Psa) from patients with celiac disease. The other group received Lactobacillus, which is found in fermented foods like yogurt.
Mice treated with Psa developed inflammation of the gut similar to the symptoms of celiac disease. Those treated with Lactobacillus were able to detoxify the gluten and remain symptom-free.
“We may be closer to understanding the way gut bacteria and opportunistic pathogens such as Psa could affect celiac disease risk. This will help us develop strategies to prevent these disorders, but more research is needed,” Dr. Verdu commented.
The study was published in the June issue of Gastroenterology.
Funding for the study was provided by the Canadian Institutes for Health Research.
Information on conflict of interest was not available.