Gastrointestinal inflammation by gut microbiota disturbance induces memory impairment in mice
Open accessAbstract
In this study, we tested our hypothesis regarding mechanistic cross-talk between gastrointestinal inflammation and memory loss in a mouse model. Intrarectal injection of the colitis inducer 2,4,6-trinitrobenzenesulfonic acid (TNBS) in mice caused colitis via activation of nuclear factor (NF)-κB and increase in membrane permeability. TNBS treatment increased fecal and blood levels of lipopolysaccharide (LPS) and the number of Enterobacteriaceae, particularly Escherichia coli (EC), in the gut microbiota composition, but significantly reduced the number of Lactobacillus johnsonii (LJ). Indeed, we observed that the mice treated with TNBS displayed impaired memory, as assessed using the Y-maze and passive avoidance tasks. Furthermore, treatment with EC, which was isolated from the feces of mice with TNBS-induced colitis, caused memory impairment and colitis, and increased the absorption of orally administered LPS into the blood. Treatment with TNBS or EC induced NF-κB activation and tumor necrosis factor-α expression in the hippocampus of mice, as well as suppressed brain-derived neurotrophic factor expression. However, treatment with LJ restored the disturbed gut microbiota composition, lowered gut microbiota, and blood LPS levels, and attenuated both TNBS- and EC-induced memory impairment and colitis. These results suggest that the gut microbiota disturbance by extrinsic stresses can cause gastrointestinal inflammation, resulting in memory impairment.
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Treatment of mice with E. coli isolated from colitic mice caused colitis and brain memory impairment.
“Moreover, the treatment of mice with E. coli, isolated from colitic mice, caused colitis and brain memory impairment (95, 96).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [95]
Treatment with L. johnsonii restored a healthy gut microbiota composition and attenuated both colitis and E. coli-induced memory impairment.
“In contrast, the treatment with L. johnsonii restored a healthy gut microbiota composition and attenuated both colitis and E. coli-induced memory impairment (95, 96).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [95]
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- Authors
- Jang, S.-E., Lim, S.-M., Jeong, J.-J., Jang, H.-M., Lee, H.-J., Han, M. J., & Kim, D.-H.
- Affiliations
- Kyung Hee University (KR)
- Corresponding author
- Kim, D-H
- ORCID
- Jang, S-E
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 11
- Issue
- 2
- Pages
- 369-379
- ISSN
- 1933-0219 (ISSN-L)
- OpenAlex
- W2625490249
- Cited by
- 190
- References
- 47
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 31 · 2023: 24 · 2022: 33 · 2021: 39 · 2020: 17 · 2019: 16 · 2018: 10
- FWCI
- 4.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation (2013M3A9B6076413)
- Ministry of Science, ICT and Future Planning (2013M3A9B6076413)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- gut microbiota, gastrointestinal inflammation, colitis, memory impairment, 2,4,6-trinitrobenzene sulfonic acid, lipopolysaccharide, Escherichia coli, Lactobacillus johnsonii, NF-κB, TNF-α, brain-derived neurotrophic factor, hippocampus, neuroinflammation, intestinal permeability
- MeSH terms
- Gastrointestinal Microbiome, Lactobacillus johnsonii, Animals, Cell Membrane Permeability, Colitis, Disease Models, Animal, Escherichia coli, Feces, Hippocampus, Humans, Inflammation, Male, Memory Disorders, Mice, Inbred ICR, Trinitrobenzenesulfonic Acid, Tumor Necrosis Factor-alpha, NF-kappa B, Gastrointestinal Tract, Mice, Dysbiosis
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