The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
Wenke Feng - One of the best experts on this subject based on the ideXlab platform.
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Attenuation of chronic-binge alcohol-induced liver injury by Lactobacillus rhamnosus GG culture supernatant via inhibition of intestinal barrier dysfunction (653.12)
The FASEB Journal, 2014Co-Authors: Min Zhang, Yuhua Wang, Yanlong Liu, Cuiqing Zhao, Craig J. Mcclain, Wenke FengAbstract:Binge drinking after chronic alcohol consumption is one of the important factors contributing to the progression of hepatic steatosis to steatohepatitis. Our previous study showed that Lactobacillus rhamnosus GG (LGG) culture supernatant (LGGs) ameliorated acute alcohol-induced liver injury. The present study investigated the effects and potential mechanisms of LGGs on chronic-binge alcohol-induced liver injury. Mice were fed Lieber DeCarli Diet containing 5% alcohol for 4 weeks, then gavaged single dose of alcohol at 5 g/kg and lasted for 6 hours. Chronic-binge alcohol exposure induced marked increase in hepatic steatosis and injury, which were attenuated by LGGs supplementation. LGGs application prevented chronic-binge alcohol-elevated intestinal permeability and circulating endotoxin level, indicating a beneficial effect of LGGs on intestinal barrier integrity. Further studies demonstrated that the effect of LGGs is through increasing intestinal tight junction proteins and proteins involved in the barr...
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Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of Lactobacillus rhamnosus GG treatment.
PloS one, 2013Co-Authors: Lara M. Bull-otterson, Yuhua Wang, Yanlong Liu, Wenke Feng, Irina A. Kirpich, Xiang Qin, Leila Gobejishvili, Swati Joshi-barve, Tulin Ayvaz, Joseph F. PetrosinoAbstract:Enteric dysbiosis plays an essential role in the pathogenesis of alcoholic liver disease (ALD). Detailed characterization of the alterations in the gut microbiome is needed for understanding their pathogenic role in ALD and developing effective therapeutic approaches using probiotic supplementation. Mice were fed liquid Lieber-DeCarli Diet without or with alcohol (5% v/v) for 6 weeks. A subset of mice were administered the probiotic Lactobacillus rhamnosus GG (LGG) from 6 to 8 weeks. Indicators of intestinal permeability, hepatic steatosis, inflammation and injury were evaluated. Metagenomic analysis of the gut microbiome was performed by analyzing the fecal DNA by amplification of the V3–V5 regions of the 16S rRNA gene and large-scale parallel pyrosequencing on the 454 FLX Titanium platform. Chronic ethanol feeding caused a decline in the abundance of both Bacteriodetes and Firmicutes phyla, with a proportional increase in the gram negative Proteobacteria and gram positive Actinobacteria phyla; the bacterial genera that showed the biggest expansion were the gram negative alkaline tolerant Alcaligenes and gram positive Corynebacterium. Commensurate with the qualitative and quantitative alterations in the microbiome, ethanol caused an increase in plasma endotoxin, fecal pH, hepatic inflammation and injury. Notably, the ethanol-induced pathogenic changes in the microbiome and the liver were prevented by LGG supplementation. Overall, significant alterations in the gut microbiome over time occur in response to chronic alcohol exposure and correspond to increases in intestinal barrier dysfunction and development of ALD. Moreover, the altered bacterial communities of the gut may serve as significant therapeutic target for the prevention/treatment of chronic alcohol intake induced intestinal barrier dysfunction and liver disease.
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Lactobacillus rhamnosus GG Treatment Potentiates Intestinal Hypoxia-Inducible Factor, Promotes Intestinal Integrity and Ameliorates Alcohol-Induced Liver Injury
The American journal of pathology, 2011Co-Authors: Yuhua Wang, Yanlong Liu, Craig J. Mcclain, Irina A. Kirpich, Shirish Barve, Wenke FengAbstract:Gut-derived endotoxin is a critical factor in the development and progression of alcoholic liver disease (ALD). Probiotics can treat alcohol-induced liver injury associated with gut leakiness and endotoxemia in animal models, as well as in human ALD; however, the mechanism or mechanisms of their beneficial action are not well defined. We hypothesized that alcohol impairs the adaptive response-induced hypoxia-inducible factor (HIF) and that probiotic supplementation could attenuate this impairment, restoring barrier function in a mouse model of ALD by increasing HIF-responsive proteins (eg, intestinal trefoil factor) and reversing established ALD. C57BJ/6N mice were fed the Lieber DeCarli Diet containing 5% alcohol for 8 weeks. Animals received Lactobacillus rhamnosus GG (LGG) supplementation in the last 2 weeks. LGG supplementation significantly reduced alcohol-induced endotoxemia and hepatic steatosis and improved liver function. LGG restored alcohol-induced reduction of HIF-2α and intestinal trefoil factor levels. In vitro studies using the Caco-2 cell culture model showed that the addition of LGG supernatant prevented alcohol-induced epithelial monolayer barrier dysfunction. Furthermore, gene silencing of HIF-1α/2α abolished the LGG effects, indicating that the protective effect of LGG is HIF-dependent. The present study provides a mechanistic insight for utilization of probiotics for the treatment of ALD, and suggests a critical role for intestinal hypoxia and decreased trefoil factor in the development of ALD.
H. Wayne Sampson - One of the best experts on this subject based on the ideXlab platform.
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Effect of Alcohol Consumption on Adult and Aged Bone: Composition, Morphology, and Hormone Levels of a Rat Animal Model
Alcoholism clinical and experimental research, 1998Co-Authors: H. Wayne Sampson, Valerie A. Hebert, Holli L. Booe, Thomas H. ChampneyAbstract:To determine the effect of life-long alcohol consumption on the adult and aged rat model, 4-week-old, female Sprague-Dawley rats were divided into three Diet groups. Alcohol-treated animals were fed a modified Lieber-DeCarli Diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid Diet in which maltose-dextrin substituted calories supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae (primarily cancellous bone) and femora (primarily cortical bone) were removed for analysis after 3, 6, 9, 12, or 18 months on the Diets. Serum was collected for analysis of calcium levels, the calcium regulating hormones; parathyroid hormone, 25-hydroxyvitamin D, calcitonin, cor-ticosterone, estradiol, testosterone, and IGF-1. Creatinine, SGOT/ AST, and SGPT/ALT levels were measured to determine kidney and liver integrity. Previous studies, with young animals, showed that chronic alcohol consumption during the age of bone development reduced bone density and bone mass in both cortical and cancellous bone. The present study demonstrates that these reductions last throughout life, whereas morphological values, such as length and diameter, attain control levels. Calcium regulating hormones and sex hormones are essentially normal and do not appear to be the primary causative agent for adult alcohol-induced osteopenia, but it appears to be due to a more direct effect of alcohol on bone cells.
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Effect of Alcohol Consumption on Adult and Aged Bone: A Histomorphometric Study of the Rat Animal Model
Alcoholism clinical and experimental research, 1998Co-Authors: H. Wayne SampsonAbstract:The adult and aged skeleton exist in a time when osteoporosis and age-related bone loss is at a maximum, and it is modified by lifestyle factors such as alcohol. To determine the effect of life-long alcohol consumption on the adult and aged rat model, 4-week-old female Sprague-Dawley rats were divided into three Diet groups. Alcohol-treated animals were fed a modified Lieber-DeCarli Diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid Diet in which maltose-dextrin substituted calories supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae were removed and prepared for histomorphometric analysis after 3, 6, 9, 12, or 18 months on the Diets. Previous studies, with young animals, showed that chronic alcohol consumption during the age of bone development reduced bone volume and trabecular number in cancellous bone. The present study demonstrates that these reductions last throughout life. The rate of bone formation is reduced in alcohol-fed animals, but most bone cell parameters are relative normal, except for wall thickness, indicating a reduced osteoblast activity.
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Alcohol consumption by young actively growing rats: a histomorphometric study of cancellous bone.
Alcoholism clinical and experimental research, 1997Co-Authors: H. Wayne Sampson, Catherine Chaffin, Jason Lange, Buren DefeeAbstract:Alcohol consumption by young actively growing rats has been previously demonstrated to decrease bone density. This study addresses the mechanism of alcohol action on the early phases of bone growth and development using histomorphometric techniques. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli Diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid Diet in which maltose-dextrin-substituted calories were supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae, including epiphyseal growth plate, were removed for analysis after 2, 4, 6, or 8 weeks on the Diets. Trabecular volume and number were greatly reduced in the alcohol-fed animals; however, bone formation rates and mineralization rates were normal. Epiphyseal growth rate and proliferation rate were essentially stopped in the alcohol-fed animals.
Yanlong Liu - One of the best experts on this subject based on the ideXlab platform.
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Fibroblast growth factor 21 deficiency exacerbates chronic alcohol-induced hepatic steatosis and injury.
Scientific reports, 2016Co-Authors: Yanlong Liu, Min Zhang, Cuiqing Zhao, Jian Xiao, Liming Liu, Cuiling Wang, Ming-hua Zheng, Yong-ping ChenAbstract:Fibroblast growth factor 21 (FGF21) is a hepatokine that regulates glucose and lipid metabolism in the liver. We sought to determine the role of FGF21 in hepatic steatosis in mice exposed to chronic alcohol treatment and to discern underlying mechanisms. Male FGF21 knockout (FGF21 KO) and control (WT) mice were divided into groups that were fed either the Lieber DeCarli Diet containing 5% alcohol or an isocaloric (control) Diet for 4 weeks. One group of WT mice exposed to alcohol received recombinant human FGF21 (rhFGF21) in the last 5 days. Liver steatosis and inflammation were assessed. Primary mouse hepatocytes and AML-12 cells were incubated with metformin or rhFGF21. Hepatic genes and the products involved in in situ lipogenesis and fatty acid β-oxidation were analyzed. Alcohol exposure increased circulating levels and hepatic expression of FGF21. FGF21 depletion exacerbated alcohol-induced hepatic steatosis and liver injury, which was associated with increased activation of genes involved in lipogenesis mediated by SREBP1c and decreased expression of genes involved in fatty acid β-oxidation mediated by PGC1α. rhFGF21 administration reduced alcohol-induced hepatic steatosis and inflammation in WT mice. These results reveal that alcohol-induced FGF21 expression is a hepatic adaptive response to lipid dysregulation. Targeting FGF21 signaling could be a novel treatment approach for alcoholic steatohepatitis.
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Attenuation of chronic-binge alcohol-induced liver injury by Lactobacillus rhamnosus GG culture supernatant via inhibition of intestinal barrier dysfunction (653.12)
The FASEB Journal, 2014Co-Authors: Min Zhang, Yuhua Wang, Yanlong Liu, Cuiqing Zhao, Craig J. Mcclain, Wenke FengAbstract:Binge drinking after chronic alcohol consumption is one of the important factors contributing to the progression of hepatic steatosis to steatohepatitis. Our previous study showed that Lactobacillus rhamnosus GG (LGG) culture supernatant (LGGs) ameliorated acute alcohol-induced liver injury. The present study investigated the effects and potential mechanisms of LGGs on chronic-binge alcohol-induced liver injury. Mice were fed Lieber DeCarli Diet containing 5% alcohol for 4 weeks, then gavaged single dose of alcohol at 5 g/kg and lasted for 6 hours. Chronic-binge alcohol exposure induced marked increase in hepatic steatosis and injury, which were attenuated by LGGs supplementation. LGGs application prevented chronic-binge alcohol-elevated intestinal permeability and circulating endotoxin level, indicating a beneficial effect of LGGs on intestinal barrier integrity. Further studies demonstrated that the effect of LGGs is through increasing intestinal tight junction proteins and proteins involved in the barr...
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Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of Lactobacillus rhamnosus GG treatment.
PloS one, 2013Co-Authors: Lara M. Bull-otterson, Yuhua Wang, Yanlong Liu, Wenke Feng, Irina A. Kirpich, Xiang Qin, Leila Gobejishvili, Swati Joshi-barve, Tulin Ayvaz, Joseph F. PetrosinoAbstract:Enteric dysbiosis plays an essential role in the pathogenesis of alcoholic liver disease (ALD). Detailed characterization of the alterations in the gut microbiome is needed for understanding their pathogenic role in ALD and developing effective therapeutic approaches using probiotic supplementation. Mice were fed liquid Lieber-DeCarli Diet without or with alcohol (5% v/v) for 6 weeks. A subset of mice were administered the probiotic Lactobacillus rhamnosus GG (LGG) from 6 to 8 weeks. Indicators of intestinal permeability, hepatic steatosis, inflammation and injury were evaluated. Metagenomic analysis of the gut microbiome was performed by analyzing the fecal DNA by amplification of the V3–V5 regions of the 16S rRNA gene and large-scale parallel pyrosequencing on the 454 FLX Titanium platform. Chronic ethanol feeding caused a decline in the abundance of both Bacteriodetes and Firmicutes phyla, with a proportional increase in the gram negative Proteobacteria and gram positive Actinobacteria phyla; the bacterial genera that showed the biggest expansion were the gram negative alkaline tolerant Alcaligenes and gram positive Corynebacterium. Commensurate with the qualitative and quantitative alterations in the microbiome, ethanol caused an increase in plasma endotoxin, fecal pH, hepatic inflammation and injury. Notably, the ethanol-induced pathogenic changes in the microbiome and the liver were prevented by LGG supplementation. Overall, significant alterations in the gut microbiome over time occur in response to chronic alcohol exposure and correspond to increases in intestinal barrier dysfunction and development of ALD. Moreover, the altered bacterial communities of the gut may serve as significant therapeutic target for the prevention/treatment of chronic alcohol intake induced intestinal barrier dysfunction and liver disease.
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Lactobacillus rhamnosus GG Treatment Potentiates Intestinal Hypoxia-Inducible Factor, Promotes Intestinal Integrity and Ameliorates Alcohol-Induced Liver Injury
The American journal of pathology, 2011Co-Authors: Yuhua Wang, Yanlong Liu, Craig J. Mcclain, Irina A. Kirpich, Shirish Barve, Wenke FengAbstract:Gut-derived endotoxin is a critical factor in the development and progression of alcoholic liver disease (ALD). Probiotics can treat alcohol-induced liver injury associated with gut leakiness and endotoxemia in animal models, as well as in human ALD; however, the mechanism or mechanisms of their beneficial action are not well defined. We hypothesized that alcohol impairs the adaptive response-induced hypoxia-inducible factor (HIF) and that probiotic supplementation could attenuate this impairment, restoring barrier function in a mouse model of ALD by increasing HIF-responsive proteins (eg, intestinal trefoil factor) and reversing established ALD. C57BJ/6N mice were fed the Lieber DeCarli Diet containing 5% alcohol for 8 weeks. Animals received Lactobacillus rhamnosus GG (LGG) supplementation in the last 2 weeks. LGG supplementation significantly reduced alcohol-induced endotoxemia and hepatic steatosis and improved liver function. LGG restored alcohol-induced reduction of HIF-2α and intestinal trefoil factor levels. In vitro studies using the Caco-2 cell culture model showed that the addition of LGG supernatant prevented alcohol-induced epithelial monolayer barrier dysfunction. Furthermore, gene silencing of HIF-1α/2α abolished the LGG effects, indicating that the protective effect of LGG is HIF-dependent. The present study provides a mechanistic insight for utilization of probiotics for the treatment of ALD, and suggests a critical role for intestinal hypoxia and decreased trefoil factor in the development of ALD.
Thomas R. Ziegler - One of the best experts on this subject based on the ideXlab platform.
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Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption
2016Co-Authors: Junqiang Tian, Lou Ann S. Brown, Dean P. Jones, Marc S. Levin, Lihua Wang, Deborah C. Rubin, Thomas R. ZieglerAbstract:Background: Alcohol consumption is associated with oxidative stress in multiple tissues in vivo, yet the effect of chronic alcohol intake on intestinal redox state has received little attention. In this study, we investigated the redox status of 2 major intracel-lular redox regulating couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion. Methods: Sprague-Dawley rats were fed the liquid Lieber-DeCarli Diet consisting of 36% ethanol of total calories for 6 weeks. Control rats were pair-fed with an isocaloric, ethanol-free liquid Diet. Defined mucosal samples from the jejunum, ileum, and colon were obtained and analyzed by high-performance liquid chromatography (HPLC) for GSH and Cys pool redox status. Mucosal free malondialdehyde (MDA) was measured as an indicator of lipid peroxidation. Results: In the ethanol-fed rats, Cys and mixed disulfide (GSH-Cys) wer
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Intestinal redox status of major intracellular thiols in a rat model of chronic alcohol consumption.
JPEN. Journal of parenteral and enteral nutrition, 2009Co-Authors: Junqiang Tian, Lou Ann S. Brown, Dean P. Jones, Marc S. Levin, Lihua Wang, Deborah C. Rubin, Thomas R. ZieglerAbstract:Background: Alcohol consumption is associated with oxidative stress in multiple tissues in vivo, yet the effect of chronic alcohol intake on intestinal redox state has received little attention. In this study, we investigated the redox status of 2 major intracellular redox regulating couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion. Methods: Sprague-Dawley rats were fed the liquid Lieber-DeCarli Diet consisting of 36% ethanol of total calories for 6 wecks. Control rats were pair-fed with an isocaloric, ethanol-free liquid Diet. Defined mucosal samples from the jejunum, ileum, and colon were obtained and analyzed by high-performance liquid chromatography (HPLC) for GSH and Cys pool redox status. Mucosal free malondialdehyde (MDA) was measured as an indicator of lipid peroxidation. Results: In the ethanol-fed rats, Cys and mixed disulfide (GSH-Cys) were significantly decreased in all 3 segments of intestinal mucosa. Free MDA was increased in jejunal but not in ileal or colonic mucosa. Chronic ethanol ingestion significantly increased mucosal GSH concentration in association with a more reducing GSH/ GSSG redox potential in the jejunum, but these indices were unchanged in the ileum. In the colon, chronic ethanol ingestion increased oxidant stress as suggested by decreased GSH and oxidized GSH/GSSG redox potential. Conclusions: Chronic alcohol intake differentially alters the mucosal redox status in proximal to distal intestinal segments in rats. Such changes may reflect different adaptability of these intestinal segments to the oxidative stress challenge induced by chronic ethanol ingestion.
Yuhua Wang - One of the best experts on this subject based on the ideXlab platform.
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Attenuation of chronic-binge alcohol-induced liver injury by Lactobacillus rhamnosus GG culture supernatant via inhibition of intestinal barrier dysfunction (653.12)
The FASEB Journal, 2014Co-Authors: Min Zhang, Yuhua Wang, Yanlong Liu, Cuiqing Zhao, Craig J. Mcclain, Wenke FengAbstract:Binge drinking after chronic alcohol consumption is one of the important factors contributing to the progression of hepatic steatosis to steatohepatitis. Our previous study showed that Lactobacillus rhamnosus GG (LGG) culture supernatant (LGGs) ameliorated acute alcohol-induced liver injury. The present study investigated the effects and potential mechanisms of LGGs on chronic-binge alcohol-induced liver injury. Mice were fed Lieber DeCarli Diet containing 5% alcohol for 4 weeks, then gavaged single dose of alcohol at 5 g/kg and lasted for 6 hours. Chronic-binge alcohol exposure induced marked increase in hepatic steatosis and injury, which were attenuated by LGGs supplementation. LGGs application prevented chronic-binge alcohol-elevated intestinal permeability and circulating endotoxin level, indicating a beneficial effect of LGGs on intestinal barrier integrity. Further studies demonstrated that the effect of LGGs is through increasing intestinal tight junction proteins and proteins involved in the barr...
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Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of Lactobacillus rhamnosus GG treatment.
PloS one, 2013Co-Authors: Lara M. Bull-otterson, Yuhua Wang, Yanlong Liu, Wenke Feng, Irina A. Kirpich, Xiang Qin, Leila Gobejishvili, Swati Joshi-barve, Tulin Ayvaz, Joseph F. PetrosinoAbstract:Enteric dysbiosis plays an essential role in the pathogenesis of alcoholic liver disease (ALD). Detailed characterization of the alterations in the gut microbiome is needed for understanding their pathogenic role in ALD and developing effective therapeutic approaches using probiotic supplementation. Mice were fed liquid Lieber-DeCarli Diet without or with alcohol (5% v/v) for 6 weeks. A subset of mice were administered the probiotic Lactobacillus rhamnosus GG (LGG) from 6 to 8 weeks. Indicators of intestinal permeability, hepatic steatosis, inflammation and injury were evaluated. Metagenomic analysis of the gut microbiome was performed by analyzing the fecal DNA by amplification of the V3–V5 regions of the 16S rRNA gene and large-scale parallel pyrosequencing on the 454 FLX Titanium platform. Chronic ethanol feeding caused a decline in the abundance of both Bacteriodetes and Firmicutes phyla, with a proportional increase in the gram negative Proteobacteria and gram positive Actinobacteria phyla; the bacterial genera that showed the biggest expansion were the gram negative alkaline tolerant Alcaligenes and gram positive Corynebacterium. Commensurate with the qualitative and quantitative alterations in the microbiome, ethanol caused an increase in plasma endotoxin, fecal pH, hepatic inflammation and injury. Notably, the ethanol-induced pathogenic changes in the microbiome and the liver were prevented by LGG supplementation. Overall, significant alterations in the gut microbiome over time occur in response to chronic alcohol exposure and correspond to increases in intestinal barrier dysfunction and development of ALD. Moreover, the altered bacterial communities of the gut may serve as significant therapeutic target for the prevention/treatment of chronic alcohol intake induced intestinal barrier dysfunction and liver disease.
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Lactobacillus rhamnosus GG Treatment Potentiates Intestinal Hypoxia-Inducible Factor, Promotes Intestinal Integrity and Ameliorates Alcohol-Induced Liver Injury
The American journal of pathology, 2011Co-Authors: Yuhua Wang, Yanlong Liu, Craig J. Mcclain, Irina A. Kirpich, Shirish Barve, Wenke FengAbstract:Gut-derived endotoxin is a critical factor in the development and progression of alcoholic liver disease (ALD). Probiotics can treat alcohol-induced liver injury associated with gut leakiness and endotoxemia in animal models, as well as in human ALD; however, the mechanism or mechanisms of their beneficial action are not well defined. We hypothesized that alcohol impairs the adaptive response-induced hypoxia-inducible factor (HIF) and that probiotic supplementation could attenuate this impairment, restoring barrier function in a mouse model of ALD by increasing HIF-responsive proteins (eg, intestinal trefoil factor) and reversing established ALD. C57BJ/6N mice were fed the Lieber DeCarli Diet containing 5% alcohol for 8 weeks. Animals received Lactobacillus rhamnosus GG (LGG) supplementation in the last 2 weeks. LGG supplementation significantly reduced alcohol-induced endotoxemia and hepatic steatosis and improved liver function. LGG restored alcohol-induced reduction of HIF-2α and intestinal trefoil factor levels. In vitro studies using the Caco-2 cell culture model showed that the addition of LGG supernatant prevented alcohol-induced epithelial monolayer barrier dysfunction. Furthermore, gene silencing of HIF-1α/2α abolished the LGG effects, indicating that the protective effect of LGG is HIF-dependent. The present study provides a mechanistic insight for utilization of probiotics for the treatment of ALD, and suggests a critical role for intestinal hypoxia and decreased trefoil factor in the development of ALD.