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Role of serotonin in the pathogenesis of inflammatory bowel disease

Serotonin (5‐Hydroxytrytamine, 5‐HT) is a major gastrointestinal paracrine hormone and enteric neurotransmitter. Although it has been known that serotonin level is increased in the inflamed gut in patients with inflammatory bowel disease (IBD) which is characterized by an excessive release of several proinflammatory cytokines, its role in the pathogenesis of IBD has not been revealed. In this study, we investigated the molecular mechanism by which serotonin aggravates intestinal inflammation. In in vitro model of intestinal inflammation, serotonin induced adhesion of monocyte to HT‐29 colon epithelial cells in a concentration‐dependent manner, which was similar to TNF‐α. However, no additive effect was seen in case of co‐treatment of the cells with serotonin and TNF‐α. Rectal administration of serotonin into normal colon did not induce inflammatory response. However, exogenous serotonin aggravated the TNBS‐induced inflammation by increasing the expressions of chemokines and adhesion molecules. The enhanced expression of IL‐8 which is a pro‐inflammatory and pro‐angiogenic agent correlated to the increased neutrophil infiltration and angiogenesis in the colon tissues co‐treated with serotonin and TNBS. In addition, serotonin itself induced angiogenesis using in vivo chick chorioallantoic membrane (CAM) assay. In conclusion, our results indicate that abnormally increased serotonin acts as a pro‐inflammatory and pro‐angiogenic factor during intestinal inflammation.