Increased Incidence of Inflammatory Bowel Disease: The Price of the Decline of Infectious Burden?

Hélène Feillet; Jean-François Bach


Curr Opin Gastroenterol. 2004;20(6) 

In This Article

Abstract and Introduction

Purpose of Review: It is now apparent that the increase in the incidence of autoimmune and allergic diseases in Western countries is explained by the decrease in infections. The question is posed to determine whether a similar explanation can be proposed for the increased incidence of inflammatory bowel disease.
Recent Findings: Studies performed in murine experimental models of inflammatory bowel disease have shown that colitis onset can be prevented by bacteria, bacterial extracts, or helminths. Particular interest was given to probiotics (either live or killed), which protect from disease in a toll-like receptor 9 dependent fashion. This protective effect involves regulatory cytokines as indicated by in vitro studies on human inflamed colonic cells. At the clinical level, there is strong suggestion but still limited proof that probiotics improve inflammatory bowel disease through immunoregulatory mechanisms.
Summary: Converging clinical and experimental data strongly suggest the protective nonspecific role of infections on inflammatory bowel disease independently from the triggering role of some specific bacteria. The extension to inflammatory bowel disease of the hygiene hypothesis opens new therapeutic perspectives including the revisiting of probiotics and other forms of exposure to bacteria or parasite components.

Converging epidemiologic data reveal a steady increase in the incidence of inflammatory bowel disease (IBD) during the last half of the twentieth century, even if a plateau has now been reached in some high-incidence areas such as northern Europe and North America.[1*,2] This increase in incidence is real but should be qualified in terms of the improvement of disease awareness and diagnosis. During the same period, an obvious trend towards the decline of infectious diseases was noted.[3]

As has been previously done for allergic and autoimmune diseases, it was tempting to hypothesize a causal relation between these two observations (according to the hygiene hypothesis). Because of decreased solicitation by infectious agents, the immune system mounts immunopathologic responses against various antigens (autoantigens, allergens, and antigens from some specific pathogens), giving rise to immune disorders.


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