Abstract
Inflammatory bowel diseases : Crohn's disease (CD) and ulcerative colitis (UC) affect more than one person in a thousand. Their etiology is multifactorial, including genetic and environmental factors. Numerous genetic risk factors with low individual impact have been identified, but alone they account for only a small proportion of the risk. Their analysis nevertheless contributes to understanding the physiology of these effectors and the involvement of cytokine signalling pathways such as TNF, IL-12 and IL-23. Associated gene expression profiling studies carried out on intestinal biopsies show the involvement of certain metabolic pathways (CD) or extracellular matrix biology (UC). The main environmental factor concerns variations in the intestinal flora, whose diversity and composition are greatly disturbed during chronic inflammatory bowel disease. The flora is poor in bacteria producing anti-inflammatory molecules - such as certain short-chain fatty acids - and, on the contrary, rich in bacteria producing pro-inflammatory products.
