Evidence map›Paper›PMID 20554880›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Pivotal role of TLR4 receptors in alcohol-induced neuroinflammation and brain damage.

Silvia Alfonso-Loeches, Maya Pascual-Lucas, Ana M Blanco, Irene Sanchez-Vera, Consuelo Guerri

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed, 1 pooled it
17.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

333 citing papers in PubMed, 1 synthesis or guideline pooled it, 574 citations in OpenAlex.

  1. Pooled it
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  9. Global deletion ofbioRxiv : the preprint server for biology · 2026
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  13. miR-146a-5p mitigates ethanol-induced neuroinflammation by targeting Btg2-dependent microglial activation.Malawi medical journal : the journal of Medical Association of Malawi · 2026
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  14. Ethanol drinking involves astrocytes in male Wistar rats.bioRxiv : the preprint server for biology · 2026
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273 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Silvia Alfonso-LoechesDepartment of Cellular Pathology, Centro de Investigación Príncipe Felipe, 46012 Valencia, Spain.
Maya Pascual-Lucas
Ana M Blanco
Irene Sanchez-Vera
Consuelo Guerri
Centro de Investigacion Principe Felipe · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors play an important role in the innate immune response, although emerging evidence indicates their role in brain injury and neurodegeneration. Alcohol abuse induces brain damage and can sometimes lead to neurodegeneration. We recently found that ethanol can promote TLR4 signaling in glial cells by triggering the induction of inflammatory mediators and causing cell death, suggesting that the TLR4 response could be an important mechanism of ethanol-induced neuroinflammation. This study aims to establish the potential role of TLR4 in both ethanol-induced glial activation and brain damage. Here we report that TLR4 is critical for ethanol-induced inflammatory signaling in glial cells since the knockdown of TLR4, by using both small interfering RNA or cells from TLR4-deficient mice, abolished the activation of microtubule-associated protein kinase and nuclear factor-kappaB pathways and the production of inflammatory mediators by astrocytes. Our results demonstrate, for the first time, that whereas chronic ethanol intake upregulates the immunoreactive levels of CD11b (microglial marker) and glial fibrillary acidic protein (astrocyte marker), and also increases caspase-3 activity and inducible nitric oxide synthase, COX-2, and cytokine levels [interleukin (IL)-1beta, tumor necrosis factor-alpha, IL-6] in the cerebral cortex of female wild-type mice, TLR4 deficiency protects against ethanol-induced glial activation, induction of inflammatory mediators, and apoptosis. Our findings support the critical role of the TLR4 response in the neuroinflammation, brain injury, and possibly in the neurodegeneration induced by chronic ethanol intake.

Indexed as

AnimalsAstrocytesBrain InjuriesCalcium-Binding ProteinsCaspase 3Central Nervous System DepressantsCyclooxygenase 2Disease Models, AnimalEncephalitisEthanolFemaleGene Expression RegulationGreen Fluorescent ProteinsInterleukin-1betaLipopolysaccharide ReceptorsLipopolysaccharidesAif1 protein, mouseCalcium-Binding ProteinsCaspase 3Central Nervous System DepressantsCyclooxygenase 2EthanolGreen Fluorescent ProteinsInterleukin-1betaLipopolysaccharide ReceptorsLipopolysaccharidesLy96 protein, mouseLymphocyte Antigen 96Microfilament ProteinsNerve Tissue ProteinsPTGS2 protein, humanRNA, MessengerRNA, Small InterferingTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID20554880
PMCPMC6634595
OpenAlexW1975931952

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.