Journal
CELL
Volume 161, Issue 2, Pages 264-276Publisher
CELL PRESS
DOI: 10.1016/j.cell.2015.02.047
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Funding
- NIH [5DP5OD017924]
- Caltech Center for Environmental Microbial Interactions Award
- National Science Foundatio (NSF) Emerging Frontiers in Research and Innovation Award [EFRI-1137089]
- National Human Genome Research Institute (NHGRI) grant [R01HG005826]
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant [DK078938]
- National Institute of Mental Health (NIMH) grant [MH100556]
- National Institute of Allergy and Infectious Diseases (NIAID) grant [AI106302]
- Food Allergy Research and Education (FARE)
- University of Chicago Digestive Diseases Center Core Grant [P30DK42086]
- Emerging Frontiers & Multidisciplinary Activities
- Directorate For Engineering [1137089] Funding Source: National Science Foundation
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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.
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