Despite the fact that the true origin of ulcerative colitis (UC) still remains elusive, basic as well as clinical research bring many new data on ethiopathogenesis of this inflammatory condition. It seems clear that UC originates from interaction of several intrinsic and extrinsic factors that contribute individually in a particular patient.
Among internal factors, the gut microbiota, intestinal epithelial cells, and components of gut immune system play the key role. Differences in the composition of microbial environment in the gut (dysbiosis) have been described in patients with UC.
Though the genome-wide association studies revealed many new susceptibility loci in UC patients, genetic testing has still no place in the routine clinical practice. Some environmental factors maycontributeto disease susceptibility, some others are associated with the risk of acute relapse in UC patients in remission.
The former group include nutrients (saturated fatty acids), smoking and appendectomy in past. The risk of acute relapse increases with psychological stress, using some drugs (i.e. non-steroidal anti-inflammatory drugs) and intercurrent infections, especially in upper respiratory tract.
The currently accepted model of the pathogenesis of UC is of an inappropriate immune response to host microorganisms in genetically susceptible people. The „hygiene" hypothesis explains the UC as a consequence of insuficient oral immunotolerance due to minimal antigenic stimulation in early childhood.
According to Maratka's "two-component" hypothesis, the primary non-specific inflammation may be superimposed by secondary "infection" originating from luminal bacteria which eventually leads to typical picture of UC.