[Etiopathogenesis of inflammatory bowel diseases].

The pathogenesis of IBD is only partly understood; various environmental and host (e.g. genetic-, epithelial-, immune and non-immune) factors are involved. It is a multifactorial polygenic disease with probable genetic heterogeneity, some genes are associated with IBD itself, while others increase the risk of ulcerative colitis (UC) or Crohn's disease (CD) or are associated with disease location and/or behaviour. The role of environmental factors, in particular, enteric antigens, smoking and non-steroid anti-inflammatory drug use has been well established. However uptil now no proof of a role of any unique pathogenic bacteria or special dietary and/or psychosocial factor has been identified. In this hypothesis, the disease may develop in a genetically predisposed host as a consequence of disregulated immune response to environmental, in particular, enteric antigens, resulting in a continuous immune-mediated inflammation (in CD predominantly Th-1, in UC a modified Th-2 mechanisms are involved) and not in tolerance. As a consequence, the permeability of mucosa and the antigen challenge increases, in contrast, the disregulated immune response is unable to downregulate the inflammatory process. This will result in a continuous inflammation and tissue damage. The pathogenesis of CD is thought to be mainly an antigen driven, T-lymphocyte dependent process, while in UC the role of epithelial factors and activated granulocytes are essential.