CLEVELAND, Sept. 21 (UPI) -- Researchers at Case Western Reserve University identified a fungus that works with two types of bacteria to cause symptoms of Crohn's disease, according to a new study.
The study is the first to find a fungus plays a role in development of the disease, and the discovery may lead to new ways of treating Crohn's, according to researchers involved with the study.
Crohn's disease is an inflammatory bowel disorder that causes inflammation of the digestive tract leading to abdominal pain, severe diarrhea and fatigue, and is one of the most common forms of inflammatory bowel disorder.
"We already know that bacteria, in addition to genetic and dietary factors, play a major role in causing Crohn's disease," Dr. Mahmoud Ghannoum, a professor and director of the Center for Medical Mycology at Case Western Reserve University and lead author of the study, said in a press release. "Essentially, patients with Crohn's have abnormal immune responses to these bacteria, which inhabit the intestines of all people. While most researchers focus their investigations on these bacteria, few have examined the role of fungi, which are also present in everyone's intestines."
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For the study, published in the journal mBio, the researchers analyzed fecal samples from 20 people with Crohn's disease and 28 of their Crohn's-free family members, as well as from 21 people who did not have the disease and neither did their family members.
In people with Crohn's, the researchers found two bacteria, E. coli and Serratia marcescens, move "in lock step" with the fungus Candida tropicalis, working to produce a biofilm that prompts inflammation typical of Crohn's disease.
The bacteria and fungus appeared in much greater concentrations in samples from patients than in their family members, and the overall bacterial and fungal makeup of samples from people without the disease or family with the disease was significantly different.
"Among hundreds of bacterial and fungal species inhabiting the intestines, it is telling that the three we identified were so highly correlated in Crohn's patients," Ghannoum said. "Furthermore, we found strong similarities in what may be called the 'gut profiles' of the Crohn's-affected families, which were strikingly different from the Crohn's-free families. We have to be careful, though, and not solely attribute Crohn's disease to the bacterial and fungal makeups of our intestines. For example, we know that family members also share diet and environment to significant degrees. Further research is needed to be even more specific in identifying precipitators and contributors of Crohn's."
