ArticleCells2023
Ethanol Induces Neuroinflammation in a Chronic Plus Binge Mouse Model of Alcohol Use Disorder via TLR4 and MyD88-Dependent Signaling.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Context-dependent effects of microglial MyD88 removal on voluntary ethanol consumption in mice.Neuropharmacology · 2026Article
- P2X7R Signaling and Differential Regulation of Neuroinflammatory and Behavior Responses in Male and Female Mice During Chronic Ethanol Exposure.International journal of molecular sciences · 2026Article
- Early abstinence in severe alcohol use disorder: MCP-1 decline, choroid plexus shrinkage, and region-specific grey-matter volume changes.Translational psychiatry · 2026Article
- Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.Frontiers in cell and developmental biology · 2026Article
- Impact of adolescent ethanol binge on serotonin signaling and pain sensitivity post-withdrawal.Alcohol (Fayetteville, N.Y.) · 2025Article
- Microglial activation drives neuronal dysregulation in alcohol-induced seizure susceptibility.Scientific reports · 2025Article
- Morphological Changes of the Retina in Alcohol Use Disorder: A Systematic Review and Meta-analysis of Studies Using Optical Coherence Tomography.Indian journal of psychological medicine · 2025Review
- Thiamine Deficiency and Neuroinflammation Are Important Contributors to Alcohol Use Disorder.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Review
- Severe alcohol use and COVID-19: implications for physical and mental health.Frontiers in psychiatry · 2025Review
- Modulation of TNFα-driven neuroinflammation by Gardenin A: insights fromFrontiers in pharmacology · 2025Article
- Integrated metabolomic-lipidomic profiling reveals novel biomarkers and therapeutic targets for alcohol use disorder with cognitive impairment.Frontiers in psychiatry · 2025Article
- Reduction of Alcohol-Dependent Lung Pathological Features in Rats Treated with Fenofibrate.International journal of molecular sciences · 2024Article
- Imaging neuroinflammation in individuals with substance use disorders.The Journal of clinical investigation · 2024Review
- Promising immunomodulators for management of substance and alcohol use disorders.Expert opinion on pharmacotherapy · 2024Review
- Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice.International journal of molecular sciences · 2024Article
- Epigenetic regulation of microglia and neurons by proinflammatory signaling following adolescent intermittent ethanol (AIE) exposure and in human AUD.Advances in drug and alcohol research · 2024Review
- Alcohol-induced structural and cellular brain alterations: molecular and histopathological mechanisms.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ethanol induces neuroinflammation, which is believed to contribute to the pathogenesis of alcohol use disorder (AUD). Toll-like receptors (TLRs) are a group of pattern recognition receptors (PRRs) expressed on both immune cells, including microglia and astrocytes, and non-immune cells in the central nervous system (CNS). Studies have shown that alcohol activates TLR4 signaling, resulting in the induction of pro-inflammatory cytokines and chemokines in the CNS. However, the effect of alcohol on signaling pathways downstream of TLR4, such as MyD88 and TRIF (TICAM) signaling, has not been evaluated extensively. In the current study, we treated male wild-type, TLR4-, MyD88-, and TRIF-deficient mice using a chronic plus binge mouse model of AUD. Evaluation of mRNA expression by qRT-PCR revealed that ethanol increased IL-1β, TNF-α, CCL2, COX2, FosB, and JunB in the cerebellum in wild-type and TRIF-deficient mice, while ethanol generally did not increase the expression of these molecules in TLR4- and MyD88-deficient mice. Furthermore, IRF3, IRF7, and IFN-β1, which are associated with the TRIF-dependent signaling cascade, were largely unaffected by alcohol. Collectively, these results suggest that the TLR4 and downstream MyD88-dependent signaling pathways are essential in ethanol-induced neuroinflammation in this mouse model of AUD.
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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.