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Host genetics of Irritable bowel syndrome: more clues towards inflammation and infection
Irritable bowel syndrome (IBS) shows a familial tendency but studying host genetic factors in this condition is fraught with difficulty due to vaguely defined phenotypes. One in five of IBS begins with an acute gastroenteritis; this is defined as post-infectious IBS (PI-IBS). Given the similarity between PI-IBS and diarrhoea-predominant IBS (IBS-D), Swan et al hypothesised that IBS-D would be characterised by a genetic tendency to overreact to infectious or inflammatory insults and to show persistent immune activation. In order to test this hypothesis, the authors carried out two studies: in the first, they assessed gene expression analysis in rectal biopsies and peripheral blood mononuclear cell cytokine production in healthy volunteers, patients 6 months after Campylobacter jejuni infection, IBS-D and IBS with constipation (IBS-C) patients. In part 2, polymorphisms in genes whose expression was altered in Part 1 were assessed in 179 HV, 179 IBS-D, 122 IBS-C and 41 PI-IBS. Mucosal expression of CCL11, CCL13, TNFSF15 and Calpain 8 was increased while NR1D1, GPR161 and GABRE was decreased in IBS. Similar patterns were seen after infection with Campylobacter jejuni. Polymorphisms in TNFSF15, previously linked to Crohn's disease, were associated with IBS with diarrhoea. Polymorphisms …
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