Serotonin is a critical signaling molecule in the gut; it is released from enterochromaffin cells initiates peristaltic, secretory, vasodilatory, vagal, and nociceptive reflexes.
In this study, doctors from North America assessed whether enteric serotonin signaling was defective in ulcerative colitis and irritable bowel syndrome (IBS).
The team obtained rectal biopsy specimens from healthy controls, as well as patients with ulcerative colitis, IBS with diarrhea (IBS-D), and IBS with constipation (IBS-C).
|Mucosal serotonin was reduced in ulcerative colitis and IBS.|
They measured elements of serotonin signaling, including measures of serotonin content, release, and reuptake.
The doctors found that mucosal serotonin, tryptophan hydroxylase 1 messenger RNA, serotonin transporter messenger RNA, and serotonin transporter immunoreactivity were all reduced in ulcerative colitis, IBS-C, and IBS-D.
They determined that the enterochromaffin cell population was decreased in severe ulcerative colitis samples.
Dr Matthew Coates and colleagues concluded, “These data show that ulcerative colitis and IBS are associated with similar molecular changes in serotonergic signaling mechanisms”.
“While ulcerative colitis and IBS have distinct pathophysiologic properties, these data suggest that shared defects in serotonin signaling may underlie the altered motility, secretion, and sensation”.
“These findings represent the first demonstration of significant molecular alterations specific to the gut in patients with IBS and support the assertion that disordered gastrointestinal function in IBS involves changes intrinsic to the bowel”.