Pathogenesis of Crohn's disease: Bug or no bug

World J Gastrointest Pathophysiol. 2015 Feb 15;6(1):1-12. doi: 10.4291/wjgp.v6.i1.1.

Abstract

The possibility of an infectious origin in inflammatory bowel disease (IBD) has been postulated since the first description of Crohn's disease (CD). Many observations implicate bacteria as a trigger for the development of CD: lesions occur in regions with higher bacterial concentrations; aphthous ulcers occur in Peyer's patches; inflammation resolves when the fecal stream is diverted and is reactivated following reinfusion of bowel contents; severity of the disease is correlated with bacterial density in the mucosa; granulomas can contain bacteria; and susceptible mice raised in germ-free conditions develop inflammation when bacteria are introduced in the 1990's, several studies sought to establish a relationship with viral infections and the onset of IBD, finally concluding that no direct link had been demonstrated. In the past fifteen years, evidence relating IBD pathogenesis to Mycobacterium avium paratuberculosis, salmonella, campylobacter, etc., has been found. The tendency now under discussion to regard microbiota as the primary catalyst has led to the latest studies on microbiota as pathogens, focusing on Escherichia coli, mainly in ileal CD. The present review discusses the literature available on these "bugs".

Keywords: Bacteria; Crohn’s disease; Inflammatory bowel disease; Pathogenesis; Ulcerative colitis; Virus.

Publication types

  • Review