ArticleJournal of neuroscience research2021
Extracellular microvesicles promote microglia-mediated pro-inflammatory responses to ethanol.
Article in Journal of neuroscience research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 52 citations in OpenAlex.
- Towards Mechanism-Informed Treatments for Mental Health.Journal of neurochemistry · 2026Review
- Ethanol Alters the Neurexin Landscape in Human Neuroblastoma Cells.Alcohol, clinical & experimental research · 2026Article
- Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol.The American journal of pathology · 2026Article
- Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Impact of adolescent ethanol binge on serotonin signaling and pain sensitivity post-withdrawal.Alcohol (Fayetteville, N.Y.) · 2025Article
- Purinergic and extracellular vesicle signaling in alcohol-induced blood-brain barrier breakdown and neuroimmune activation.Brain, behavior, and immunity · 2025Review
- Physiological Mechanisms Vulnerable to Alcohol-Induced Alterations: Role in Chronic Comorbidities.Comprehensive Physiology · 2025Review
- Microglia promote neurodegeneration and hyperkatifeia during withdrawal and prolonged abstinence from binge alcohol.bioRxiv : the preprint server for biology · 2025Article
- Behavioral and Brain Gene and Protein Changes in Female Mice Consuming Ethanol During Pregnancy and Lactation.Biomolecules · 2025Article
- Thiamine Deficiency and Neuroinflammation Are Important Contributors to Alcohol Use Disorder.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Role of extracellular vesicle-mediated neurodegeneration in substance use disorders.Current opinion in physiology · 2025Article
- Alcohol-Induced Changes in Brain Microstructure: Uncovering Novel Pathophysiological Mechanisms of AUD Using Translational DTI in Humans and Rodents.Current topics in behavioral neurosciences · 2025Review
- Impact of Neuroimmune System Activation by Adolescent Binge Alcohol Exposure on Adult Neurobiology.Advances in experimental medicine and biology · 2025Review
- GET73 modulates lipopolysaccharide- and ethanol-induced increase in cytokine/chemokine levels in primary cultures of microglia of rat cerebral cortex.Pharmacological reports : PR · 2024Article
- Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by AβJournal of neuroinflammation · 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
- Adolescent alcohol drinking interaction with the gut microbiome: implications for adult alcohol use disorder.Advances in drug and alcohol research · 2024Article
- Aging Microglia and Their Impact in the Nervous System.Advances in neurobiology · 2024Review
- Alcohol, HMGB1, and Innate Immune Signaling in the Brain.Alcohol research : current reviews · 2024Review
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol use disorder (AUD) pathology features pro-inflammatory gene induction and microglial activation. The underlying cellular processes that promote this activation remain unclear. Previously considered cellular debris, extracellular vesicles (EVs) have emerged as mediators of inflammatory signaling in several disease states. We investigated the role of microvesicles (MVs, 50 nm-100 µm diameter EVs) in pro-inflammatory and microglial functional gene expression using primary organotypic brain slice culture (OBSC). Ethanol caused a unique immune gene signature that featured: temporal induction of pro-inflammatory TNF-α and IL-1β, reduction of homeostatic microglia state gene Tmem119, progressive increases in purinergic receptor P2RY12 and the microglial inhibitory fractalkine receptor CX3CR1, an increase in the microglial presynaptic gene C1q, and a reduction in the phagocytic gene TREM2. MV signaling was implicated in this response as reduction of MV secretion by imipramine blocked pro-inflammatory TNF-α and IL-1β induction by ethanol, and ethanol-conditioned MVs (EtOH-MVs) reproduced the ethanol-associated immune gene signature in naïve OBSC slices. Depletion of microglia prior to ethanol treatment prevented pro-inflammatory activity of EtOH-MVs, as did incubation of EtOH-MVs with the HMGB1 inhibitor glycyrrhizin. Ethanol caused HMGB1 secretion from cultured BV2 microglia in MVs through activation of PI3 kinase. In summary, these studies find MVs modulate pro-inflammatory gene induction and microglial activation changes associated with ethanol. Thus, MVs may represent a novel therapeutic target to reduce neuroinflammation in the setting of alcohol abuse or other diseases that feature a neuroimmune component. [Correction added on 5 April 2021, after first online publication: The copyright line was changed.].
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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.