The lab is excited to share our latest research, published today in PLoS Pathogens. Using a mouse model of Crohn’s disease, the lab discovered that acute gastroenteritis caused by common food-poisoning bacteria accelerates the growth of adherent-invasive E. coli (AIEC) – a bacterium that has been linked to Crohn’s disease.
Western societies have a disproportionately high rate of inflammatory bowel disease (IBD), with growing incidence especially in the adolescent population. A large body of evidence supports the view that bacteria in the gut participate in the pathophysiology of human bowel diseases. The unifying concept is chronic inflammation that is driven by microbial stimulation of the mucosal immune system. However, the mechanisms by which pathogenic or commensal microbes work in concert with each other and with host responses to perpetuate this inflammation is not well known. Adherent-invasive E. coli (AIEC) are Crohn’s disease (CD)-associated bacteria that are implicated in disease pathology. AIEC are pro-inflammatory and may play a central role in maintaining chronic inflammation in response to other CD risk factors, such as acute infectious gastroenteritis. Here, we show that indeed, acute infectious gastroenteritis creates an inflammatory environment in the gut that drives AIEC expansion and worsens disease severity. The increase in disease severity strictly correlates with this AIEC bloom because blocking this bloom by sensitizing AIEC to host defenses also improves the health status of the host. The long time period between recovery from acute gastroenteritis and new onset CD may allow for targeted interventions to mitigate the risk of CD in AIEC-positive individuals.