The pathogenesis and etiology of inflammatory bowel disease (IBD) is poorly understood. As a matter of fact, it is not even certain whether either one is a single entity with different forms of clinical manifestations, or whether each one represents a single clearly separable entity. Common features of both diseases are chronic persistence, recurrent exacerbation and remission, the production of autoantibodies, as well as the expression of aberrant HLA-class II molecules on the surface of epithelial cells on the site of inflammation gut. It is likely that these events involve a disturbed immunoregulatory function or autoimmune process. Since the beginning of investigation the cause of IBD, infectious agents (bacteria, virus, mycobacterium paratuberculosis and others) or bacterial products (endotoxin, peptidoglycans from the bacterial cell wall) have been considered as primary causes. Epidemiological studies showed a marked increase of the incidence rates of IBD in industrial countries leading to the hypothesis, that environmental factors could play a role in the pathogenesis of the disease. So far it is clear that the major identified risk factor for IBD is a genetic susceptibility confirmed by studies showing a positive family history.