People who retain a particular bacterium in their gut after a bout of food poisoning may be at an increased risk of developing Crohn’s disease later in life, according to a new study led by researchers at McMaster University.

Using a mouse model of Crohn’s disease, the researchers discovered that acute infectious gastroenteritis caused by common food-poisoning bacteria accelerates the growth of adherent-invasive E. coli (AIEC) — a bacterium that has been linked to the development of Crohn’s.

Even after the mice had eliminated the food-poisoning bacteria, researchers still observed increased levels of AIEC in the gut, which led to worsened symptoms over a long period of time.

The study, published in the journal PLOS Pathogens, was funded by grants from the Canadian Institutes of Health Research and Crohn’s and Colitis Canada.

Crohn’s disease is a debilitating bowel disease characterized by the inflammation of the intestines. Today, one in every 150 Canadians is living with Crohn’s or colitis, a rate that ranks among the highest worldwide.

“This is a lifelong disease that often strikes people in their early years, leading to decades of suffering, an increased risk of colorectal cancer, and an increased risk of premature death,” said Brian Coombes, senior author of the study. At McMaster University he is a professor of biochemistry and biomedical sciences and a researcher at the Michael G. DeGroote Institute for Infectious Disease Research.

The study’s results, said Coombes, means that new diagnostic tools should be developed to identify AIEC-colonized individuals who may be at greater risk for Crohn’s disease following an episode of acute infectious gastroenteritis.

“We need to understand the root origins of this disease — and to use this information to invigorate a new pipeline of treatments and preventions. It has never been more pressing.”

Acute infectious gastroenteritis potentiates a Crohn’s Disease pathobiont to fuel ongoing inflammation in the post-infectious period

PLoS Pathogen, 6.oct.16, http://dx.doi.org/10.1371/journal.ppat.1005907

http://journals.plos.org/plospathogens/article?id=10.1371%2Fjournal.ppat.1005907&utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+plospathogens%2FNewArticles+(PLOS+Pathogens+-+New+Articles)

Crohn’s disease (CD) is a chronic inflammatory condition of diverse etiology. Exposure to foodborne pathogens causing acute gastroenteritis produces a long-term risk of CD well into the post-infectious period but the mechanistic basis for this ongoing relationship to disease onset is unknown. We developed two novel models to study the comorbidity of acute gastroenteritis caused by Salmonella Typhimurium or Citrobacter rodentium in mice colonized with adherent-invasive Escherichia coli (AIEC), a bacterial pathobiont linked to CD. Here, we show that disease activity in the post-infectious period after gastroenteritis is driven by the tissue-associated expansion of the resident AIEC pathobiont, with an attendant increase in immunopathology, barrier defects, and delays in mucosal restitution following pathogen clearance. These features required AIEC resistance to host defense peptides and a fulminant inflammatory response to the enteric pathogen. Our results suggest that individuals colonized by AIEC at the time of acute infectious gastroenteritis may be at greater risk for CD onset. Importantly, our data identify AIEC as a tractable disease modifier, a finding that could be exploited in the development of therapeutic interventions following infectious gastroenteritis in at-risk individuals.