Feillet Hélène, Bach Jean-François
Necker Hospital, Paris, France.
Curr Opin Gastroenterol. 2004 Nov;20(6):560-4. doi: 10.1097/00001574-200411000-00010.
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.
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.
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.