ArticleAddiction biology2018
Chronic ethanol consumption: role of TLR3/TRIF-dependent signaling.
Article in Addiction biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- EFFECTS OF TOLL-LIKE RECEPTOR 3 - DEPENDENT IMMUNE ACTIVATION IN MICE ARE SEX- AND TISSUE- SPECIFIC: IMPLICATIONS FOR ALCOHOL USE DISORDER.bioRxiv : the preprint server for biology · 2026Article
- The need to incorporate polysubstance use in neuropsychopharmacology research: Biological lessons and new opportunities.Addiction neuroscience · 2026Article
- Purinergic and extracellular vesicle signaling in alcohol-induced blood-brain barrier breakdown and neuroimmune activation.Brain, behavior, and immunity · 2025Review
- Neuroimmune regulation of the prefrontal cortex tetrapartite synapse.Neuropharmacology · 2025Review
- Central amygdala neuroimmune signaling in alcohol use disorder.Addiction neuroscience · 2025Article
- Role of Ferroptosis in ALD: Focusing on Hepcidin and Besides Hepcidin.Current medicinal chemistry · 2025Review
- Novel medications for problematic alcohol use.The Journal of clinical investigation · 2024Review
- Knockdown of Tlr3 in dorsal striatum reduces ethanol consumption and acute functional tolerance in male mice.Brain, behavior, and immunity · 2024Article
- Neuroimmune modulators as novel pharmacotherapies for substance use disorders.Brain, behavior, & immunity - health · 2024Article
- Activation of STING signaling aggravates chronic alcohol exposure-induced cognitive impairment by increasing neuroinflammation and mitochondrial apoptosis.CNS neuroscience & therapeutics · 2024Article
- Effects of repeated alcohol abstinence on within-subject prefrontal cortical gene expression in rhesus macaques.Advances in drug and alcohol research · 2024Article
- Alcohol, HMGB1, and Innate Immune Signaling in the Brain.Alcohol research : current reviews · 2024Review
- Article
- Review
- Potential Benefits of Epidermal Growth Factor for Inhibiting Muscle Degrative Markers in Rats with Alcoholic Liver Damage.International journal of molecular sciences · 2023Article
- Chronic ethanol induces a pro-inflammatory switch in interleukin-1β regulation of GABAergic signaling in the medial prefrontal cortex of male mice.Brain, behavior, and immunity · 2023Article
- Neuroimmune pathways as targets to reduce alcohol consumption.Pharmacology, biochemistry, and behavior · 2023Article
- Toll-like receptor-mediated neuroinflammation: relevance for cognitive dysfunctions.Trends in pharmacological sciences · 2022Review
- Increased alcohol self-administration following repeated Toll-like receptor 3 agonist treatment in male and female rats.Pharmacology, biochemistry, and behavior · 2022Article
- Prenatal and adolescent alcohol exposure programs immunity across the lifespan: CNS-mediated regulation.Pharmacology, biochemistry, and behavior · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chronic ethanol consumption stimulates neuroimmune signaling in the brain, and Toll-like receptor (TLR) activation plays a key role in ethanol-induced inflammation. However, it is unknown which of the TLR signaling pathways, the myeloid differentiation primary response gene 88 (MyD88) dependent or the TIR-domain-containing adapter-inducing interferon-β (TRIF) dependent, is activated in response to chronic ethanol. We used voluntary (every-other-day) chronic ethanol consumption in adult C57BL/6J mice and measured expression of TLRs and their signaling molecules immediately following consumption and 24 hours after removing alcohol. We focused on the prefrontal cortex where neuroimmune changes are the most robust and also investigated the nucleus accumbens and amygdala. Tlr mRNA and components of the TRIF-dependent pathway (mRNA and protein) were increased in the prefrontal cortex 24 hours after ethanol and Cxcl10 expression increased 0 hour after ethanol. Expression of Tlr3 and TRIF-related components increased in the nucleus accumbens, but slightly decreased in the amygdala. In addition, we demonstrate that the IKKε/TBK1 inhibitor Amlexanox decreases immune activation of TRIF-dependent pathway in the brain and reduces ethanol consumption, suggesting the TRIF-dependent pathway regulates drinking. Our results support the importance of TLR3 and the TRIF-dependent pathway in ethanol-induced neuroimmune signaling and suggest that this pathway could be a target in the treatment of alcohol use disorders.
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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.