Critical role of TLR4 response in the activation of microglia induced by ethanol
Open accessAbstract
Microglial cells are the primary immune effector cells in the brain and play a pivotal role in the neuroinflammatory processes associated with a variety of neurological and pathological disorders. Alcohol consumption induces brain damage, although the neuropathological processes are poorly understood. We previously suggested that ethanol promotes inflammatory processes in the brain, up-regulating inflammatory mediators and signaling pathways associated with IL-1RI/TLR4 receptors. In the present study we investigate whether ethanol induces microglia activation by stimulating TLR4 response and whether this response causes neuronal death and contributes to ethanol-induced neuroinflammatory damage. We demonstrate that ethanol activates microglía and stimulates NF-kappaB, MAPKs, and MyD88-independent (IFN regulatory factor-3, IFN-beta) pathways to trigger the production of inflammatory mediators, causing neuronal death. The inflammatory response induced by ethanol is completely abrogated in microglia of TLR4-deficient mice (TLR4(-/-)), thus supporting the role of these receptors in microglia activation and neuronal death. In accord with the in vitro findings, acute ethanol administration induces microglia activation (CD11b(+) cells) in cerebral cortex of TLR4(+/+) mice, but not in TLR4(-/-) mice. Taken together, our results not only provide the first evidence of the critical role of the TLR4 response in the ethanol-induced microglia activation, but also new insight into the basic mechanisms participating in ethanol-induced neuroinflammatory damage.
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In microglia taken from TLR4 deficient mice, alcohol-induced microglial activation markers, NF-κB activation, and PIC production are absent.
“Fernandez-Lizarbe et al. (2009) found all of these to be absent in microglia taken from TLR4 deficient mice.”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Fernandez-Lizarbe et al., 2009
TLR4 knockout and knockdown with siRNAs block alcohol-induced neuroinflammatory responses in vivo.
“TLR4 knockout (Fernandez-Lizarbe et al., 2009) and knockdown with siRNAs (Alfonso-Loeches et al., 2010) also blocked alcohol-induced neuroinflammatory responses in vivo.”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Fernandez-Lizarbe et al., 2009
In vitro, brief exposure to alcohol at physiological concentrations (50 nM) induces inflammatory processes in microglia.
“In vitro, even a brief exposure to alcohol at physiological concentrations (50 nM) induces inflammatory processes in astrocytes (Blanco et al., 2005) and microglia (Fernandez-Lizarbe et al., 2009).”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Fernandez-Lizarbe et al., 2009
Chronic alcohol exposure in vivo activates microglia and astrocytes.
“Chronic exposure to alcohol in vivo activates microglia and astrocytes (Fernandez-Lizarbe et al., 2009)”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Fernandez-Lizarbe et al., 2009
As few as three daily doses of alcohol (4 g/kg i.g. in mice) induce microglial activation in the cortex.
“as few as three daily doses of alcohol (4 g/kg i.g. in mice, Fernandez-Lizarbe et al., 2009) have been reported to induce microglial activation in cortex.”
From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Fernandez-Lizarbe et al., 2009
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- Authors
- Fernandez-Lizarbe, S., Pascual, M., & Guerri, C.
- Affiliations
- Department of Cellular Pathology, Centro de Investigación Príncipe Felipe , Valencia,
- Centro de Investigacion Principe Felipe (ES)
- ORCID
- Guerri, Consuelo
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-10-01
- Volume
- 183
- Issue
- 7
- Pages
- 4733-4744
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2145136979
- Cited by
- 373
- References
- 70
- Citations by year
- 2026: 9 · 2025: 27 · 2024: 20 · 2023: 17 · 2022: 20 · 2021: 29 · 2020: 32 · 2019: 22 · 2018: 25 · 2017: 31 · 2016: 28 · 2015: 16 · 2014: 29 · 2013: 26 · 2012: 20
- FWCI
- 8.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- TLR4, microglial activation, ethanol, neuroinflammation, neuronal cell death, NF-κB signaling, MAPK signaling, MyD88-independent pathway, interferon-beta, IL-1 receptor, TLR4-deficient mice, cerebral cortex, alcohol-induced brain damage
- MeSH terms
- Ethanol, Animals, Animals, Newborn, Cells, Cultured, Female, Injections, Intraperitoneal, Mice, Inbred C57BL, Neurons, Cell Death, Rats, Wistar, Microglia, Mice, Knockout, Inflammation Mediators, Toll-Like Receptor 4, Mice, Rats
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