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Brain gut microbiome interactions and functional bowel disorders
Open accessAbstract
Alterations in the bidirectional interactions between the intestine and the nervous system have important roles in the pathogenesis of irritable bowel syndrome (IBS). A body of largely preclinical evidence suggests that the gut microbiota can modulate these interactions. A small and poorly defined role for dysbiosis in the development of IBS symptoms has been established through characterization of altered intestinal microbiota in IBS patients and reported improvement of subjective symptoms after its manipulation with prebiotics, probiotics, or antibiotics. It remains to be determined whether IBS symptoms are caused by alterations in brain signaling from the intestine to the microbiota or primary disruption of the microbiota, and whether they are involved in altered interactions between the brain and intestine during development. We review the potential mechanisms involved in the pathogenesis of IBS in different groups of patients. Studies are needed to better characterize alterations to the intestinal microbiome in large cohorts of well-phenotyped patients, and to correlate intestinal metabolites with specific abnormalities in gut-brain interactions.
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“Both neural (vagus) and hormonal (HPA axis) lines of communication combine to allow brain to influence the activities of intestinal functional effector cells, such as immune cells, epithelial cells, enteric neurons, smooth muscle cells, interstitial cells of Cajal, and enterochromaffin cells (32).”
From Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders (2018) · cites this paper as [32]
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“Mechanistic data provided mainly by animal studies highlight that probiotics exert a direct antinociceptive action through the modulation of bacterial metabolites production (i.e., neurotransmitters, neuroactive substances including GABA and serotonin) on sensitive nerve endings in the gut mucosa [2631,130]”
From Gut microbiota role in irritable bowel syndrome: New therapeutic strategies (2016) · cites this paper as [130]
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Metadata
- Authors
- Mayer, E. A., Savidge, T., & Shulman, R. J.
- Affiliations
- University of California, Los Angeles (US)
- Baylor College of Medicine (US)
- Corresponding author
- Mayer, Emeran A.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 146
- Issue
- 6
- Pages
- 1500-1512
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC4114504
- OpenAlex
- W2014965759
- Cited by
- 496
- References
- 146
- Citations by year
- 2026: 23 · 2025: 38 · 2024: 36 · 2023: 39 · 2022: 55 · 2021: 50 · 2020: 48 · 2019: 48 · 2018: 42 · 2017: 39 · 2016: 31 · 2015: 37 · 2014: 10
- FWCI
- 6.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (DK 64531, DK 48351)
- National Institute of Nursing Research (13497, AI100914, DK56338)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Infant Health and Development
- Keywords
- gut-brain axis, gut microbiota, irritable bowel syndrome, dysbiosis, functional bowel disorders, prebiotics, probiotics, antibiotics, intestinal metabolites, pathogenesis
- MeSH terms
- Animals, Anti-Inflammatory Agents, Anti-Bacterial Agents, Bacteria, Brain, Humans, Intestinal Mucosa, Intestines, Neural Pathways, Inflammatory Bowel Diseases, Signal Transduction, Probiotics, Host-Pathogen Interactions, Microbiota, Dysbiosis
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