Format

Send to

Choose Destination
Cell. 2015 Apr 9;161(2):264-76. doi: 10.1016/j.cell.2015.02.047.

Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis.

Author information

1
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
2
Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
3
Department of Pathology and Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
4
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. Electronic address: ehsiao@caltech.edu.

Erratum in

  • Cell. 2015 Sep 24;163:258.

Abstract

The gastrointestinal (GI) tract contains much of the body's serotonin (5-hydroxytryptamine, 5-HT), but mechanisms controlling the metabolism of gut-derived 5-HT remain unclear. Here, we demonstrate that the microbiota plays a critical role in regulating host 5-HT. Indigenous spore-forming bacteria (Sp) from the mouse and human microbiota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the mucosa, lumen, and circulating platelets. Importantly, microbiota-dependent effects on gut 5-HT significantly impact host physiology, modulating GI motility and platelet function. We identify select fecal metabolites that are increased by Sp and that elevate 5-HT in chromaffin cell cultures, suggesting direct metabolic signaling of gut microbes to ECs. Furthermore, elevating luminal concentrations of particular microbial metabolites increases colonic and blood 5-HT in germ-free mice. Altogether, these findings demonstrate that Sp are important modulators of host 5-HT and further highlight a key role for host-microbiota interactions in regulating fundamental 5-HT-related biological processes.

PMID:
25860609
PMCID:
PMC4393509
DOI:
10.1016/j.cell.2015.02.047
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center