The role of major virulence factors and pathogenicity of adherent-invasive Escherichia coli in patients with Crohn's disease

Abstract

Inflammatory bowel disease (IBD) is a term that describes Crohn's disease (CD) and ulcerative colitis (UC), and these two conditions are characterised by chronic inflammation of the gastrointestinal tract. Dysbiosis of intestinal microbiota has been consistently linked to patients with IBD. In the last two decades, the progressive implication of adherent-invasive Escherichia coli (AIEC) pathogenesis in patients with CD has been increasing. Here we discuss recent findings that indicate the role and mechanisms of AIEC in IBD. We also highlight AIEC virulence factor genes and mechanisms that suggest an important role in the severity of inflammation in CD patients. Finally, we emphasise data on the prevalence of AIEC in CD patients.

Keywords: Crohn’s disease; Escherichia coli; adherent-invasive Escherichia coli; inflammatory bowel disease; virulence factors.

Figure 1

The diagram shows changes in the gut during inflammation mediated by adherent-invasive Escherichia coli (AIEC) colonisation. Inflammation of the human gut can be triggered by several factors including diet, antibiotic administration, acute gastroenteritis, and host genetics. The pro-inflammation in human gut mediates noticeable changes in the gut, which can appear as hypoferremia and over-expression of carcinoembryonic antigen-related cell adhesion molecule (CEACAM6) surface receptors produced by epithelial cells in human gut. AIEC strains have been evolved and gained a competitive advantage in inflamed gut of the human intestines. This evolution includes the ability of AIEC strains to use a modified f imH protein to bind to CEACAM6 and to be able to utilise amine (N) and sulphur (S) oxides as electron acceptors AIEC – adherent-invasive Escherichia coli, CEACAM6 – carcinoembryonic antigen-related cell adhesion molecule, Th – T helper, IL – interleukin, TNF-α – tumour necrosis factor α, IFN-γ – interferon γ.