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Neuroinflammation is implicated in the pathogenesis of alcohol use disorders. We investigated the role of Gut-Brain interactions in alcohol-induced neuroinflammation by probiotic-mediated manipulation of intestinal dysbiosis in mice. Chronic ethanol feeding induced dysbiosis, as evidenced by an increase in Firmicutes/Bacteroidetes ratio and depletion of  Lactobacillus  species in the colon. Ethanol increased the levels of IL-1β, IL-6, and TNFα in plasma and the mRNA for  IL-1β ,  IL-6 ,  TNFα , and  MCP1  genes in the cerebral cortex and hippocampus. Ethanol feeding increased inulin flux from the circulation into different brain regions, accompanied by the increase in TLR4 mRNA levels in the cerebral cortex and hippocampus. The immunofluorescence confocal microscopy showed that ethanol elevates the expression of microglial activation marker TMEM119 in the cerebral cortex. Feeding  L. plantarum  suppressed the ethanol-induced dysbiosis to some extent, as evidenced by attenuation of ethanol effects on Firmicutes/Bacteroidetes ratio and abundance of  Lactobacillus spp .  L. plantarum  blocked ethanol-induced elevation of plasma cytokines, inulin permeability to the brain, mRNA for  TLR4 ,  IL-1β ,  IL-6 ,  TNFα , and  MCP1  in brain regions, and the expression of TMEM119 in the cerebral cortex. The  L. plantarum  effect was absent in mice that express a dominant-negative EGFR, suggesting that the EGFR receptor plays an essential role in the protective effect of  L. plantarum  against ethanol-induced neuroinflammation.  L. plantarum , when administered after chronic ethanol-induced injury, rescued the ethanol-induced systemic inflammation and neuroinflammation. This study demonstrates that  L. plantarum  in the gut prevents and mitigates ethanol-induced neuroinflammation by an EGFR-dependent mechanism.

Prevention and mitigation of alcohol-induced neuroinflammation by Lactobacillus plantarum by an EGF receptor-dependent mechanism