ArticleThe international journal of neuropsychopharmacology2017
NLRP3 Inflammasome Contributes to Lipopolysaccharide-induced Depressive-Like Behaviors via Indoleamine 2,3-dioxygenase Induction.
Article in The international journal of neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Natural antidepressants in neuroimmunomodulation: molecular mechanisms, action targets, and therapeutic potential.Frontiers in immunology · 2025Pooled it
- What Animal Models Can Tell Us About Long-Term Psychiatric Symptoms in Sepsis Survivors: a Systematic Review.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Pooled it
- Sex and stress paradigm influence behavioural, neuroimmune, and microbiome responses in pubertal CD-1 mice.Brain, behavior, & immunity - health · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Analysis of the correlation between the expression levels of caspase-1/IL-1β in the peripheral blood and clinical efficacy in patients with first-episode MDD.Annals of general psychiatry · 2026Article
- Lactobacillus reuteri DSM 17,938 ameliorates LPS-induced depression-like and anxiety-like behaviors by modulating gut microbiota and brain metabolic function.Gut pathogens · 2025Article
- Interaction between depressive state and high-fat diet and its impact on behavioral and body weight changes in male mice.Scientific reports · 2025Article
- Nasal administration of mitochondria relieves depressive- and anxiety-like behaviors in male mice exposed to restraint stress through the suppression ROS/NLRP3/caspase-1/IL-1β signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Global trends of purinergic receptors and depression: A bibliometric analysis from 2003 to 2023.World journal of psychiatry · 2025Article
- The antidepressant effects of kaji-ichigoside F1 via activating PPAR-γ/CX3CR1/Nrf2 signaling and suppressing NF-κB/NLRP3 signaling pathways.Frontiers in pharmacology · 2025Article
- Review
- Review
- Major depressive disorder: hypothesis, mechanism, prevention and treatment.Signal transduction and targeted therapy · 2024Review
- Mechanistic insights into the anti-depressant effect of curcumin based on network pharmacology and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Hycanthone Inhibits Inflammasome Activation and Neuroinflammation-Induced Depression-Like Behaviors in Mice.Biomolecules & therapeutics · 2023Article
- NLRP3 Inflammasome: From Pathophysiology to Therapeutic Target in Major Depressive Disorder.International journal of molecular sciences · 2022Review
- Exosome Biogenesis and Lysosome Function Determine Podocyte Exosome Release and Glomerular Inflammatory Response during Hyperhomocysteinemia.The American journal of pathology · 2022Article
- NLRP3/caspase-1/GSDMD-mediated pyroptosis exerts a crucial role in astrocyte pathological injury in mouse model of depression.JCI insight · 2021Article
- Agmatine as a novel candidate for rapid-onset antidepressant response.World journal of psychiatry · 2021Review
- Sick for science: experimental endotoxemia as a translational tool to develop and test new therapies for inflammation-associated depression.Molecular psychiatry · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Inflammation may play a significant role in the pathogenesis of depression, although the molecular target for the treatment of inflammation-mediated depressive symptoms remains to be elucidated. Recent studies have implicated the NLRP3 inflammasome in various psychiatric disorders, including depression. However, the underlying mechanism by which NLRP3 inflammasome activation mediates the progression of depressive-like behaviors remains poorly understood. Methods: We examined whether NLRP3 deficiency influenced depressive-like behaviors and cerebral inflammation following systemic administration of lipopolysaccharide in mice. To further assess the contribution of the NLRP3 inflammasome to the progression of depression, we evaluated the effects of NLRP3 signaling on levels of indoleamine 2,3-dioxygenase. Results: Nlrp3-deficient mice exhibited significant attenuation of depressive-like behaviors and cerebral caspase-1 activation in a lipopolysaccharide-induced model of depression. Treatment with the antidepressant amitriptyline failed to block NLRP3-dependent activation of caspase-1, but inhibited lipopolysaccharide-promoted production of interleukin-1β mRNA via suppressing NF-κB signaling in mouse mixed glial cultures. Interestingly, lipopolysaccharide administration produced NLRP3-dependent increases in indoleamine 2,3-dioxygenase expression and activity of mouse brain. Furthermore, inflammasome-activating stimulations, but not treatment with the inflammasome product interleukin-1β, triggered indoleamine 2,3-dioxygenase mRNA induction in mixed glial cells. Conclusions: Our data indicate that the NLRP3 inflammasome is significantly implicated in the progression of systemic inflammation-induced depression. NLRP3-dependent caspase-1 activation produced significant increases in indoleamine 2,3-dioxygenase levels, which may play a significant role in lipopolysaccharide-induced depression. Collectively, our findings suggest that indoleamine 2,3-dioxygenase is a potential downstream mediator of the NLRP3 inflammasome in inflammation-mediated depressive-like behaviors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.