AJP - GI Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 296: G685-G695, 2009. First published December 18, 2008; doi:10.1152/ajpgi.90685.2008
0193-1857/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
296/3/G685    most recent
90685.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bischoff, S. C.
Right arrow Articles by Gershon, M. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bischoff, S. C.
Right arrow Articles by Gershon, M. D.

NEUROREGULATION AND MOTILITY

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

Stephan C. Bischoff,1,2,4 Reiner Mailer,2 Oliver Pabst,3 Gisela Weier,2 Wanda Sedlik,4 Zhishan Li,4 Jason J. Chen,4 Dennis L. Murphy,5 and Michael D. Gershon4

1Department of Nutritional Medicine and Immunology, University of Hohenheim, Stuttgart, Germany; 2Department of Gastroenterology, Hepatology, and Endocrinology, and 3Department of Immunology, University Medical School of Hannover, Hannover, Germany; 4Department of Anatomy and Cell Biology, Columbia University, New York, New York; and 5National Institute of Mental Health, Laboratory of Clinical Science, National Institutes of Health, Bethesda, Maryland

Submitted 4 December 2008 ; accepted in final form 10 December 2008

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.

neutrophils; motility; inflammatory bowel disease; epithelial cells


Address for reprint requests and other correspondence: S. C. Bischoff, Dept. of Nutritional Medicine and Immunology, Univ. of Hohenheim, D-70593 Stuttgart, Germany (e-mail: bischoff.stephan{at}uni-hohenheim.de)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.