Stress may be the culprit behind Crohn’s disease, study finds

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Researchers have identified a possible link between psychological stress and Crohn’s disease.

In a study led by Canada’s McMaster University and the Farncombe Family Digestive Health Research Institute, and published in the journal Nature, the authors said that mouse models found that stress hormones suppressed the innate immune system that normally protects the gut from Enterobacteriaceae. 

Enterobacteriaceae is a group of bacteria, including E. coli, which has been linked to the inflammatory disease of the gastrointestinal tract.

In people with Crohn’s disease, harmless bacteria present in the GI tract are mistaken for foreign invaders and the immune system mounts a response, causing the inflammation.

“Clinical evidence implicates periods of psychological stress in Crohn’s disease exacerbation, and disturbances in the gut microbiome might contribute to the pathogenic mechanism,” the authors wrote. “Here we show that stress-exposed mice develop ileal dysbiosis, dominated by the expansion of Enterobacteriaceae.”

According to Science Direct, dybosis is defined as an “imbalance” in the gut microbial community that is associated with disease.

A woman clutches her stomach
(Credit: iStock)

However, without properly functioning immune cells, the epithelial cellular wall can break down and allow microbes associated with Crohn’s disease to invade the gut and trigger symptom flare-ups.

“The main takeaway is that psychological stress impedes the body’s ability to fight off gut bacteria that may be implicated in Crohn’s disease. Innate immunity is designed to protect us from microbes that do not belong in the gut, like harmful bacteria,” senior author Brian Coombes, professor and chair of biochemistry and biomedical sciences at McMaster, said in a statement.

“When our innate immune system functions properly, it prevents harmful bacteria from colonizing us, but when it breaks down, it leaves an opening for pathogens to colonize locations they normally cannot and cause illness,” he added. 

Coombes said that by removing stress hormones in the mouse models, it restored proper function to immune cells and epithelial cells, blocking the invasion of harmful microbes.

“Overall, our study shows that psychological stress creates a beneficial environment for [adherent-invasive E. coli (AIEC)], a [Crohn’s]-associated pathobiont in the gut. Given that the pathological changes observed following psychological stress are augmented in the presence of AIEC, this work establishes a rationale for future studies to dissect the relative contributions of the microbiome and psychological stress on the gut environment,” the study concludes. “In our current study, AIEC appears to derive this benefit by evading host nutritional immunity while taking advantage of an impaired induction of IL-22-mediated host defenses that rely on antimicrobial proteins and barrier maintenance. Thus, in the presence of pathobionts that efficiently evade nutritional immunity, this aberrant stress-induced host response provides a promiscuous niche for their unregulated expansion.”

“The more we know about what triggers Crohn’s disease, the closer we come to new treatments and potentially even disease prevention,” Coombes concluded, noting that the findings are still at the pre-clinical stage.

The Crohn’s & Colitis Foundation reports that men and women are equally likely to be affected and that the disease is most prevalent people between the ages of 15 and 35. 

Diet is known to aggravate Crohn’s disease and recent research suggests hereditary, genetic and environmental factors.

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