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Chronic alcohol-induced neuroinflammation involves CCR2/5-dependent peripheral macrophage infiltration and microglia
Patrick P Lowe1, Caroline Morel2, Aditya Ambade1
1Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Journal of Neuroinflammation
|October 10, 2020
Summary
Chronic alcohol consumption drives peripheral macrophage infiltration into the brain via the CCL2-CCR2 axis. Blocking this pathway with cenicriviroc (CVC) reduced neuroinflammation and restored microglia function.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Chronic alcohol use causes neuroinflammation, neuronal damage, and behavioral changes.
- Alcohol-induced neuroinflammation involves increased pro-inflammatory cytokines and microglial activation.
- Peripheral immune cell infiltration into the central nervous system (CNS) is a potential consequence of alcohol consumption.
Purpose of the Study:
- To investigate if chronic alcohol consumption leads to peripheral immune cell infiltration into the CNS.
- To determine if blocking the CCL2-CCR2 signaling pathway with cenicriviroc (CVC) can prevent alcohol-induced macrophage infiltration and alter neuroinflammation.
- To assess the impact of CVC on microglia activation and function.
Main Methods:
- C57BL/6J female mice were fed ethanol or control diets for 6 weeks, with some receiving daily CVC injections.
- Flow cytometry and reporter mice (CX3CR1eGFP/+ CCR2RFP/+) were used to characterize microglia and infiltrating macrophages.
- Gene expression analysis (Nanostring inflammation panel) and immunofluorescence were employed to evaluate neuroinflammation and microglia activation.
Main Results:
- Chronic alcohol consumption increased microglia activation and peripheral macrophage infiltration, particularly in the hippocampus.
- CVC treatment prevented alcohol-induced macrophage recruitment and partially reversed microglia activation.
- Ethanol upregulated pro-inflammatory markers in the brain, which was reduced by CVC treatment, while microglia function was restored.
Conclusions:
- Chronic alcohol consumption promotes peripheral macrophage recruitment into the CNS and alters microglia via the CCR2/5 axis.
- The CCR2/5 axis represents a potential therapeutic target for mitigating alcohol-associated neuroinflammation.
- Further research into CCR2/5 axis modulation could lead to novel treatments for alcohol-related brain damage.
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