Impact of TLR4 on behavioral and cognitive dysfunctions associated with alcohol-induced neuroinflammatory damage

  title={Impact of TLR4 on behavioral and cognitive dysfunctions associated with alcohol-induced neuroinflammatory damage},
  author={Mar{\'i}a Pascual and Pablo P{\'e}rez Bali{\~n}o and Silvia Alfonso-Loeches and Carlos M. G. Aragon and Consuelo Guerri},
  journal={Brain, Behavior, and Immunity},

Figures from this paper

Impact of the Innate Immune Response in the Actions of Ethanol on the Central Nervous System.

Evidence that indicates the participation of TLRs and the inflammasome NLRs signaling response in many effects of EtOH on the CNS, such as neuroinflammation associated with brain damage, cognitive and behavioral dysfunction, and adolescent brain development alterations is focused on.

Role of neuroinflammation in ethanol neurotoxicity

Neuroimmune Function and the Consequences of Alcohol Exposure

Models of alcohol abuse have identified significant frontal cortical degeneration and loss of hippocampal neurogenesis, consistent with neuroimmune activation pathology contributing to these alcohol-induced, long-lasting changes in the brain.



Pivotal Role of TLR4 Receptors in Alcohol-Induced Neuroinflammation and Brain Damage

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

Ethanol intake enhances inflammatory mediators in brain: role of glial cells and TLR4/IL-1RI receptors.

It is proposed that at low physiologically relevant concentrations, ethanol facilitates TLR4/IL-1RI recruitment into lipid rafts microdomains, leading to the activation and signaling of these receptors, which are important targets of ethanol-induced inflammatory brain damage.

Critical Role of TLR4 Response in the Activation of Microglia Induced by Ethanol1

It is demonstrated that ethanol activates microglía and stimulates NF-κB, MAPKs, and MyD88-independent (IFN regulatory factor-3, IFN-β) pathways to trigger the production of inflammatory mediators, causing neuronal death.

Increased systemic and brain cytokine production and neuroinflammation by endotoxin following ethanol treatment

Investigating the interaction of liver, serum and brain cytokines as well as whether ethanol would potentiate endotoxin responses once ethanol had cleared found that ethanol induced differential anti-inflammatory cytokine IL-10 responses in liver and brain could cause long lasting disruption of cytokine cascades that could contribute to protection or increased risk of multiple chronic diseases.

Toll-like receptors in neurodegeneration

NOS2 Gene Deficiency Protects from Sepsis-Induced Long-Term Cognitive Deficits

The importance of the NOS2 activation for long-term cerebral changes after severe sepsis is outlined, which is independent of the cerebral glucose uptake as evidenced by 18F-Fluordeoxyglucose small animal positron emission tomography.

Involvement of TLR4/Type I IL-1 Receptor Signaling in the Induction of Inflammatory Mediators and Cell Death Induced by Ethanol in Cultured Astrocytes1

It is shown that glial cells are stimulated by ethanol, up-regulating cytokines and inflammatory mediators associated with TLR4 and IL-1RI signaling pathways in brain, suggesting that ethanol may contribute to brain damage via inflammation.

Evidence that oxidative stress is linked to anxiety-related behaviour in mice

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Increased cytokine activity induces adaptive change that supports sensitization of ethanol withdrawal-induced anxiety that may be linked to GABAA-receptor function, and administration of the benzodiazepine receptor antagonist flumazenil before the LPS or TNF treatments prevented anxiety sensitization.