Abstract

Ulcerative colitis (UC) is a chronic and relapsing inflammatory disease of the large bowel characterized by dysregulation of the immune mucosal response, an imbalance in the synthesis and release of cytokines, and an unresolved inflammatory process associated with mucosal damage (Schirbel & Fiocchi, 2010). Although the exact mechanisms of the development of UC have not been established yet, it is known that both genetic predisposition and environmental factors are playing important roles. There is the strong evidence that environmental factors are involved in the pathogenesis of UC. The incidence of UC has increased dramatically between 1940s and the 1980s. More recent data show that, in several developed countries, UC incidence decreases in the last years (Binder, 2004). On the other hand, at the same time, the incidence of UC increased in countries where it formally was low (e.g. developing countries and developed countries in Asia, such as Japan and Korea). It is believed that factors associated with 'Westernization' may be conditioning the expression of UC. The increased incidence of UC among migrants from the low-incidence to high-incidence areas within the same or next generation confirms a strong environmental influence (Bernstein & Shanahan, 2008). Another evidence for the role of environmental factors in UC comes from twin studies: disease concordance in monozygotic twins is only 19% in UC, as opposed to 50% in Crohn's disease (CD). This observation suggests that the environmental influence is stronger in UC than in CD (Halfvarson et al., 2003). In the last decades several environmental factors, and especially the diet and the changes of the gut microbiota have been studied to improve our understanding of increased incidence of inflammatory bowel disease (IBD) in the last years and also to elucidate the pathogenesis of the disease.

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