Microbiota-derived metabolite Indoles induced aryl hydrocarbon receptor activation and inhibited neuroinflammation in APP/PS1 mice
Open accessAbstract
Gut microbiota alterations might affect the development of Alzheimer's disease (AD) through microbiota-derived metabolites. For example, microbiota-derived Indoles via tryptophan metabolism prevented Aβ accumulation and Tau hyperphosphorylation, restored synaptic plasticity, and then promoted the cognitive and behavioral ability of APP/PS1 mice. The imbalanced compositions of Indoles-producing bacteria with tryptophan deficiency were found in male APP/PS1 mice, but the molecular mechanisms remained unclear. Our current study revealed that Indoles (including indole, indole-3-acetic acid and indole-3-propionic acid) upregulated the production of aryl hydrocarbon receptor (AhR), inhibited the activation of the NF-κB signal pathway as well as the formation of the NLRP3 inflammasome, reduced the release of inflammatory cytokines, including TNF-α, IL-6, IL-1β and IL-18, alleviating the inflammatory response of APP/PS1 mice. These findings demonstrated the roles of Indoles-producing bacteria in activating the AhR pathway to regulate neuroinflammation of AD through gut microbiota-derived Indoles, which implied a novel way for AD treatment.
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Administration of an indole mixture attenuates microglial reactivity and neuroinflammation in APP/PS1 mice by activating microglial AHR signaling and inhibiting NLRP3 inflammasomes, leading to reduced amyloid-beta deposition, diminished tau hyperphosphorylation, and improved cognitive function.
“The administration of an indole mixture (indole, indole-3-acetic acid, and indole-3-propionic acid) attenuated the microglial reactivity and neuroinflammation by activating microglial AHR signaling and inhibiting NLRP3 inflammasomes. Consequently, the treatment led to reduced Aβ deposition, diminished tau hyperphosphorylation and improved cognitive function (Fig. 3d).426”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [426]
Oral gavage with a mixture of indole, indole-3-acetic acid, and indole-3-propionic acid reversed intestinal barrier impairment, reduced Aβ accumulation and tau hyperphosphorylation, leading to improved synaptic plasticity and cognitive function of APP/PS1 mice.
“oral gavage with a mixture of indole, indole-3-acetic acid, and indole-3-propionic acid reversed the intestinal barrier impairment, reduced Aβ accumulation and tau hyperphosphorylation, leading to improved synaptic plasticity and cognitive function of APP/PS1 mice.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [426]
APP/PS1 mice have significant alterations in indole-producing bacteria, coupled with intestinal barrier dysfunction and cognitive dysfunction.
“A recent study has highlighted significant alterations in indole-producing bacteria in APP/PS1 mice, which were coupled with intestinal barrier dysfunction and cognitive dysfunction.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [426]
Indoles inhibited microglial activation and NLRP3 inflammasome activation by activating microglial AHR.
“the indoles inhibited microglial activation and NLRP3 inflammasome activation by activating microglial AHR.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [426]
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
Loh, J. S., Mak, W. Q., Tan, L. K. S., Ng, C. X., Chan, H. H., Yeow, S. H., Foo, J. B., Ong, Y. S., How, C. W., & Khaw, K. Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01743-1 · Cited by 1,193 · see citing works
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- Authors
- Sun, J., Zhang, Y., Kong, Y., Ye, T., Yu, Q., Kumaran Satyanarayanan, S., Su, K.-P., & Liu, J.
- Affiliations
- Wenzhou Medical University (CN)
- China Medical University (TW)
- Corresponding author
- Su, Kuan-Pin
- Liu, Jiaming
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2022-11
- Volume
- 106
- Pages
- 76-88
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W4291674129
- Cited by
- 255
- References
- 61
- Citations by year
- 2026: 81 · 2025: 89 · 2024: 50 · 2023: 33 · 2022: 2
- FWCI
- 27.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain Behavior and Immunity (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- China Medical University Hospital
- China Medical University, Taiwan (CMU 110-AWARD-02, CMU108-SR-106, CMU110-N-17, CMU1110-SR-73, CRS-108-048, DMR-102-076, DMR-103-084, DMR-106-225, DMR-107-204, DMR-108-216, DMR-109-102, DMR-109-244, DMR-110-124, DMR-111-245, DMR-HHC-109-11, DMR-HHC-109-12, DMR-HHC-110-10, DMR-HHC-111-8)
- Tainan Municipal An-Nan Hospital
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- gut microbiota, indole, aryl hydrocarbon receptor, neuroinflammation, Alzheimer's disease, APP/PS1 mice, tryptophan metabolism, NF-κB signaling, NLRP3 inflammasome, inflammatory cytokines, indole-3-acetic acid, indole-3-propionic acid, gut microbiota metabolites
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Neuroinflammatory Diseases, Alzheimer Disease, Animals, Disease Models, Animal, Indoles, Male, Mice, Transgenic, Tryptophan, Tumor Necrosis Factor-alpha, Interleukin-6, NF-kappa B, Amyloid beta-Protein Precursor, Receptors, Aryl Hydrocarbon, Interleukin-18, Mice, Presenilin-1, Inflammasomes, Microbiota
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