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Review
. 2019 May 27:2019:9097276.
doi: 10.1155/2019/9097276. eCollection 2019.

Probiotics for Alleviating Alcoholic Liver Injury

Zelin Gu  1 , Yanlong Liu  2 , Shumeng Hu  1 , Ying You  1 , Jiaqi Wen  1 , Wancong Li  1 , Yuhua Wang  1   3   4
Affiliations
Review

Probiotics for Alleviating Alcoholic Liver Injury

Zelin Gu et al. Gastroenterol Res Pract. .

Abstract

Many animal experiments and clinical trials showed that probiotics are effective for the treatment of alcoholic liver disease. Alcohol disrupts the composition of intestinal flora; probiotics modulate the gut microbiota and reverse alcohol-associated intestinal barrier dysfunction by decreasing intestinal mucosal permeability and preventing intestinal bacteria from translocating. Probiotics enhance immune responses and reduce the levels of alcohol-induced inflammatory cytokines and reactive oxygen species (ROS) production in the liver and intestine. Probiotics also increase fatty acid β-oxidation and reduce lipogenesis, combating alcohol-induced hepatic steatosis. In this review, we summarize the current knowledge regarding the mechanism of action of probiotics for reducing the effects of alcoholic liver disease.

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Figures

Figure 1
Figure 1
The effect of alcohol on the gut-liver axis. Alcohol significantly changes intestinal microbiota diversity, reduces intestinal epithelial tight junction protein expression, and increases intestinal mucosal permeability, leading to barrier dysfunction and endotoxin translocated into the blood, inducing inflammatory cytokine and ROS production in the intestine and liver, causing hepatic steatosis and inflammation. Alcohol disorders the gut microbiota and decreases AhR ligand and IL-22 production. Alcohol exposure increased intestinal miR122a expression, decreasing occludin expression.
Figure 2
Figure 2
Probiotics function in gut-liver mechanisms. Probiotics and related products prevent ethanol-induced effects in the intestine and the liver via multiple mechanisms: (1) enhancement of antioxidant activity; (2) reduction of inflammatory cytokine expression; (3) hepatic AMPK and induction of lipid metabolism; (4) enhancement of intestinal tight junction ZO-1, claudin-1, and occludin expression via increased intestinal HIF signaling; (5) inhibition of miR122a expression leading to occludin upregulation; (6) activation of EGFR and preservation of barrier function in intestinal epithelial cells; and (7) positive modification of gut microbiota and increase AhR ligands.
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