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1 Gastrointestinal, Neuroscience and Mucosal Inflammation Research GroupsDepartment of Physiology and Biophysics, University of Calgary, Calgary, AB, Canada
2 Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: ksharkey{at}ucalgary.ca.
Enteroendocrine cells act as sensory transducers, releasing serotonin (5-HT) and numerous peptides that are involved in regulating motility, secretion and gut sensation. The action of mucosal 5-HT is terminated by a serotonin reuptake transporter (SERT). In this study we examined the hypothesis that ileitis leads to changes in enteroendocrine cell populations and mucosal serotonin availability. Ileitis was induced in guinea pigs by intraluminal injection of 2,4,6- trinitrobenzene sulfonic acid (TNBS) and experiments were conducted 3, 7 and 14 days after treatment. The number of somatostatin, neurotensin and 5-HT-immunoreactive cells increased at 3 and 7 days of ileitis, respectively, whereas no significant changes in the numbers of cholecystokinin, glucagon like peptide-2, glucose- dependent insulinotropic peptide and peptide YY- immunoreactive cells were observed. Chemical stimulation of the inflamed mucosa with sodium deoxycholic acid significantly increased 5-HT release compared to basal release. Mechanical stimulation of the mucosa potentiated the effect of the chemical stimuli at day 7. Epithelial SERT immunoreactivity was significantly reduced during the time course of inflammation. Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to the altered motility and secretion associated with intestinal inflammation by disrupting mucosal signaling to enteric nerves involved in peristaltic and secretory reflexes.
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