Cited by 206Inflammatory Bowel DiseaseGastrointestinal motility and disordersTryptophan and brain disorders

Role of serotonin in intestinal inflammation: Knockout of serotonin reuptake transporter exacerbates 2,4,6-trinitrobenzene sulfonic acid colitis in mice

Bischoff, Stephan C., Mailer, Reiner, Pabst, Oliver, Weier, Gisela, Sedlik, Wanda, Li, Zhishan, Chen, Jason J., Murphy, Dennis L. +1 more·2009·American Journal of Physiology-Gastrointestinal and Liver Physiology

Abstract

Serotonin (5-HT) regulates peristaltic and secretory reflexes in the gut. The serotonin reuptake transporter (SERT; SLC6A4), which inactivates 5-HT, is expressed in the intestinal mucosa and the enteric nervous system. Stool water content is increased and colonic motility is irregular in mice with a targeted deletion of SERT. We tested the hypotheses that 5-HT plays a role in regulating intestinal inflammation and that the potentiation of serotonergic signaling that results from SERT deletion is proinflammatory. Rectal installation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) was used to induce an immune-mediated colitis, which was compared in SERT knockout mice and littermate controls. Intestinal myeloperoxidase and histamine levels were significantly increased, whereas the survival rate and state of health were significantly decreased in TNBS-treated mice that lacked SERT. Deletion of SERT thus increases the severity of TNBS colitis. These data suggest that 5-HT and its SERT-mediated termination play roles in intestinal immune/inflammatory responses in mice.

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Crossref · 10.1152/ajpgi.90685.2008

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  • Higher levels of 5-HT in children with ASD can be linked to intestinal inflammation and play an important role in intestinal inflammatory responses, indicating a connection between enteric serotonin production and dysbiosis.

    “Lastly, higher levels of 5′-HT in children with ASD can be linked to intestinal inflammation and play an important role in intestinal inflammatory responses [200], so there is a connection between enteric serotonin production and dysbiosis.”

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Authors
Bischoff, S. C., Mailer, R., Pabst, O., Weier, G., Sedlik, W., Li, Z., Chen, J. J., Murphy, D. L., & Gershon, M. D.
Affiliations
University of Hohenheim (DE)
Venue
American Journal of Physiology-Gastrointestinal and Liver Physiology
Published
2009-03
Volume
296
Issue
3
Pages
G685-G695
ISSN
  • 0193-1857 (ISSN-L)
  • 1522-1547
OpenAlex
W1997066133
Cited by
206
References
63
Citations by year
2026: 4 · 2025: 9 · 2024: 14 · 2023: 11 · 2022: 13 · 2021: 15 · 2020: 17 · 2019: 8 · 2018: 17 · 2017: 13 · 2016: 18 · 2015: 8 · 2014: 14 · 2013: 9 · 2012: 14
FWCI
4.13
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
serotonin, serotonin transporter, intestinal inflammation, TNBS-induced colitis, immune-related colitis, enteric nervous system, myeloperoxidase, histamine, colonic motility, serotonergic signaling, knockout mice
MeSH terms
Animals, Colitis, Colon, Gastrointestinal Motility, Histamine, Mice, Inbred C57BL, Peroxidase, Rectum, Serotonin, Trinitrobenzenesulfonic Acid, Mice, Knockout, Serotonin Plasma Membrane Transport Proteins, Mice

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