NLRP3 inflammasome activation contributes to long-term behavioral alterations in mice injected with lipopolysaccharide
Open accessAbstract
Lipopolysaccharide (LPS) might affect the central nervous system by causing neuroinflammation, which subsequently leads to brain damage and dysfunction. In this study, we evaluated the role of nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation in long-term behavioral alterations of 8-week-old male C57BL/6 mice injected intraperitoneally with LPS (5mg/kg). At different time points after injection, we assessed locomotor function with a 24-point neurologic deficit scoring system and the rotarod test; assessed recognition memory with the novel object recognition test; and assessed emotional abnormality (anhedonia and behavioral despair) with the tail suspension test, forced swim test, and sucrose preference test. We also assessed protein expression of NLRP3, apoptosis-associated speck-like protein (ASC), and caspase-1 p10 in hippocampus by Western blotting; measured levels of interleukin (IL)-1β, IL-18, tumor necrosis factor α (TNFα), and IL-10 in hippocampus; measured TNFα and IL-1β in serum by ELISA; and evaluated microglial activity in hippocampus by Iba1 immunofluorescence. We found that LPS-injected mice displayed long-term depression-like behaviors and recognition memory deficit; elevated expression of NLRP3, ASC, and caspase-1 p10; increased levels of IL-1β, IL-18, and TNFα; decreased levels of IL-10; and increased microglial activation. These effects were blocked by the NLRP3 inflammasome inhibitor Ac-Tyr-Val-Ala-Asp-chloromethylketone. The results demonstrate proof of concept that NLRP3 inflammasome activation contributes to long-term behavioral alterations in LPS-exposed mice, probably through enhanced inflammation, and that NLRP3 inflammasome inhibition might alleviate peripheral and brain inflammation and thereby ameliorate long-term behavioral alterations in LPS-exposed mice.
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Endotoxin-induced DLB model exhibits NLRP3 inflammasome activation, particularly in the hippocampus.
“Endotoxin-induced DLB model also exhibits NLRP3 inflammasome activation, particularly in the hippocampus (20, 21).”
From Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway (2019) · cites this paper as [21]
Selective inhibition of the NLRP3 inflammasome with systemic treatment using Ac-YVAD-CMK exhibited anti-inflammatory and antidepressant effects.
“selective inhibition of the NLRP3 inflammasome with systemic treatment using Ac-YVAD-CMK, exhibited anti-inflammatory and antidepressant effects [157,158]”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [157]
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- Authors
- Zhu, W., Cao, F.-S., Feng, J., Chen, H.-W., Wan, J.-R., Lu, Q., & Wang, J.
- Affiliations
- Johns Hopkins University (US)
- Xiangyang Central Hospital (CN)
- Tongji Hospital (CN)
- Corresponding author
- Wang, Jian
- ORCID
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2017-02
- Volume
- 343
- Pages
- 77-84
- ISSN
- 0306-4522 (ISSN-L)
- PMC
- PMC5349320
- OpenAlex
- W2559769511
- Cited by
- 134
- References
- 61
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 15 · 2023: 13 · 2022: 18 · 2021: 17 · 2020: 19 · 2019: 12 · 2018: 10 · 2017: 9
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01AT007317, R01NS078026)
- Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medicine
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- NLRP3 inflammasome, lipopolysaccharide, neuroinflammation, behavioral alterations, depression-like behavior, memory impairment, hippocampus, microglial activation, caspase-1, IL-1β, IL-18, TNF-α, IL-10, inflammasome inhibition, long-term behavioral effects
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Amino Acid Chloromethyl Ketones, Animals, Anti-Inflammatory Agents, Depressive Disorder, Hippocampus, Lipopolysaccharides, Male, Memory Disorders, Mice, Inbred C57BL, Random Allocation, Microglia, Inflammasomes
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