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Dig Dis Sci (2013) 58:33793381 DOI 10.1007/s10620-013-2936-y
EDITORIAL
The Overlap in the Genetic Pathogenesis of Ulcerative Colitis and Irritable Bowel Syndrome
Takeshi Kamiya
Published online: 14 November 2013 Springer Science+Business Media New York 2013
Ulcerative colitis (UC) is a chronic, relapsing inammatory disorder of the gastrointestinal tract. Although the etiology of UC remains unclear, genetic and environmental factors may contribute to its pathogenesis. Several genetic studies in Western and Eastern countries have reported associations between a number of polymorphisms and UC risk.
Irritable bowel syndrome (IBS) is one of the most common chronic functional bowel disorders in which abnormal discomfort or pain is associated with defecation or a change in bowel habits, in the absence of other disease that can explain such symptoms. Although geneenvironment studies on IBS are lacking, disturbed gastrointestinal motility, dysbiosis of the colonic microbiome, sensory hypersensitivity, and psychosomatic factors have been attributed etiological signicance.
Consensus exists that a shift in the hostgut microbial relationship leading to low-grade mucosal inammation is contributory. IBS subjects have an increased number of inammatory cells, including mast cells and lymphocytes, in mucosal biopsy samples obtained from the colon, rectum, and terminal ileum. Half of the patients with IBS have microscopic intestinal and colonic inammation consistent with microscopic colitis. Moreover, acute infectious gastroenteritis is now recognized as an etiological factor for symptom development in a subset of patients with IBS, a condition termed post-infectious IBS (PI-IBS).
The main regulators of motor and sensory function of the gastrointestinal tract and a sentry cell guarding against invading microbes, mucosal mast cells are the most extensively studied immune cells in relation to IBS. The number of mast cells was signicantly greater in the terminal ileum, cecum, colon, and rectum of the patients with IBS than in that of the healthy control groups [1, 2]. The concentration of mast cell mediators such as histamine, protease, and tryptase in supernatants from mucosal biopsies of patients with IBS was higher than in those from control groups. The release of these mediators may contribute to visceral hypersensitivity by activating the enteric nervous and sensory pain pathways.
The neurotransmitter 5-hydroxytryptamine (5-HT) is present in enterochromafn (EC) cells of the gastrointestinal mucosal epithelium or the serotonergic neurons of the enteric nervous system. 5-HT released from...