The role of neuroimmune signaling in alcoholism
Open accessAbstract
Alcohol consumption and stress increase brain levels of known innate immune signaling molecules. Microglia, the innate immune cells of the brain, and neurons respond to alcohol, signaling through Toll-like receptors (TLRs), high-mobility group box 1 (HMGB1), miRNAs, pro-inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons. Repeated cycles of alcohol and stress cause a progressive, persistent induction of HMGB1, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote reward seeking behavior and increase risk of developing alcohol use disorders. Studies employing anti-oxidant, anti-inflammatory, anti-depressant, and innate immune antagonists further link innate immune gene expression to addiction-like behaviors. Innate immune molecules are novel targets for addiction and affective disorders therapies. This article is part of the Special Issue entitled "Alcoholism".
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Repeated adolescent alcohol exposure can cause neuroinflammation via the release of pro-inflammatory cytokines, which can disrupt synaptic plasticity and lead to neuropathology and cell death.
“Of equal importance is that repeated AAE can cause neuroinflammation via the release of pro-inflammatory cytokines, which can disrupt synaptic plasticity and lead to neuropathology and cell death [37–39].”
From Consequences of adolescent drug use (2023) · cites this paper as [39]
Section 5 reports that alcohol induces pro-inflammatory cytokines and that repeated exposure enhances neuroimmune signaling; Section 4 says excessive cytokines can disrupt neuronal plasticity. Section 11 reports persistent neuroimmune-marker changes after adolescent ethanol exposure. The copy does not establish the full claimed sequence—from repeated adolescent exposure through cytokine release and disrupted plasticity to neuropathology and cell death—in that adolescent setting. (LLM, conf=0.84)
Experimental — accuracy not yet measuredInteractions between the immune system and stress system associated with the withdrawal/negative affect stage involve both microglia and astrocytes.
“Interactions between the immune system and stress system that are associated with the withdrawal/negative affect stage involve both microglia and astrocytes (Crews et al., 2017).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Crews et al., 2017
Section 3 says stress affects both microglia and astrocytes, and Section 5 says immune signaling contributes to the withdrawal/negative affect stage. The paper does not specifically link both cell types to immune–stress interactions during that stage. (LLM, conf=0.82)
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References 243 · Cited by 321
Research works printed but not linked: 1
- Alfonso-Loeches, 2010, Pivotal role of TLR4 receptors in alcohol-induced neuroinflammation and brain damage, J. Neurosci. official J. Soc. Neurosci., 30, 8285, 10.1523/JNEUROSCI.0976-10.2010 · DOI · Paper page
- Authors
- Crews, F. T., Lawrimore, C. J., Walter, T. J., & Coleman, L. G.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Coleman, Leon G.
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 122
- Pages
- 56-73
- ISSN
- 0028-3908 (ISSN-L)
- PMC
- PMC5493978
- OpenAlex
- W2584378493
- Semantic Scholar
- 9d9f3b3aeb47928184e23a32efeb2a07a0fc56e3
- Cited by
- 321
- References
- 243
- Citations by year
- 2026: 30 · 2025: 39 · 2024: 29 · 2023: 40 · 2022: 36 · 2021: 38 · 2020: 38 · 2019: 30 · 2018: 27 · 2017: 14
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIAAA (AA019767, AA11605, AA007573, AA021040)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- neuroimmune signaling, alcoholism, microglia, Toll-like receptors, HMGB1, microRNA, inflammatory cytokines, stress, impulsivity, anxiety, craving, ventral striatum, reward seeking, innate immunity, anti-inflammatory therapy
- MeSH terms
- Alcoholism, Animals, Brain, Encephalitis, Humans, Neurons, Stress, Psychological, Neuroimmunomodulation, Signal Transduction, Behavior, Addictive, Microglia, HMGB1 Protein, Toll-Like Receptors
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