Alcohol or Gut Microbiota: Who Is the Guilty?
Alcoholic liver disease (ALD), a disorder caused by excessive alcohol intake represents a global health care burden. ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The su...
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| description | Alcoholic liver disease (ALD), a disorder caused by excessive alcohol intake represents a global health care burden. ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The susceptibility of alcoholic patients to develop ALD is highly variable and its progression to more advanced stages is strongly influenced by several hits (i.e., amount and duration of alcohol abuse). Among them, the intestinal microbiota and its metabolites have been recently identified as paramount in ALD pathophysiology. Ethanol abuse triggers qualitative and quantitative modifications in intestinal flora taxonomic composition, mucosal inflammation, and intestinal barrier derangement. Intestinal hypermeability results in the translocation of viable pathogenic bacteria, Gram-negative microbial products, and pro-inflammatory luminal metabolites into the bloodstream, further corroborating the alcohol-induced liver damage. Thus, the premise of this review is to discuss the beneficial effect of gut microbiota modulation as a novel therapeutic approach in ALD management. |
| doi_str_mv | 10.3390/ijms20184568 |
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ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The susceptibility of alcoholic patients to develop ALD is highly variable and its progression to more advanced stages is strongly influenced by several hits (i.e., amount and duration of alcohol abuse). Among them, the intestinal microbiota and its metabolites have been recently identified as paramount in ALD pathophysiology. Ethanol abuse triggers qualitative and quantitative modifications in intestinal flora taxonomic composition, mucosal inflammation, and intestinal barrier derangement. Intestinal hypermeability results in the translocation of viable pathogenic bacteria, Gram-negative microbial products, and pro-inflammatory luminal metabolites into the bloodstream, further corroborating the alcohol-induced liver damage. Thus, the premise of this review is to discuss the beneficial effect of gut microbiota modulation as a novel therapeutic approach in ALD management.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms20184568</identifier><identifier>PMID: 31540133</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alcohol ; Alcoholism - genetics ; Alcoholism - immunology ; Alcoholism - microbiology ; Alcoholism - physiopathology ; Animals ; Anti-Bacterial Agents - adverse effects ; Bacteria ; Bile Acids and Salts - metabolism ; Cecum ; Diet ; Dietary Supplements - microbiology ; Dysbacteriosis ; Dysbiosis - immunology ; Dysbiosis - metabolism ; Ethanol ; Ethnicity ; Fecal Microbiota Transplantation ; Feces ; Gastrointestinal Microbiome - physiology ; Gene expression ; Gram-positive bacteria ; Hepatitis ; Hepatocytes - metabolism ; Homeostasis ; Humans ; Inflammation ; Injuries ; Intestinal microflora ; Intestine ; Intestines - microbiology ; Irritable bowel syndrome ; Liver - metabolism ; Liver - physiopathology ; Liver diseases ; Liver Diseases, Alcoholic - immunology ; Liver Diseases, Alcoholic - metabolism ; Liver Diseases, Alcoholic - microbiology ; Liver Diseases, Alcoholic - physiopathology ; Metabolism ; Metabolites ; Microbiota ; Microorganisms ; Oats ; Permeability ; Physiology ; Proteins ; Review ; Small intestine</subject><ispartof>International journal of molecular sciences, 2019-09, Vol.20 (18), p.4568</ispartof><rights>2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). 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ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The susceptibility of alcoholic patients to develop ALD is highly variable and its progression to more advanced stages is strongly influenced by several hits (i.e., amount and duration of alcohol abuse). Among them, the intestinal microbiota and its metabolites have been recently identified as paramount in ALD pathophysiology. Ethanol abuse triggers qualitative and quantitative modifications in intestinal flora taxonomic composition, mucosal inflammation, and intestinal barrier derangement. Intestinal hypermeability results in the translocation of viable pathogenic bacteria, Gram-negative microbial products, and pro-inflammatory luminal metabolites into the bloodstream, further corroborating the alcohol-induced liver damage. Thus, the premise of this review is to discuss the beneficial effect of gut microbiota modulation as a novel therapeutic approach in ALD management.</description><subject>Alcohol</subject><subject>Alcoholism - genetics</subject><subject>Alcoholism - immunology</subject><subject>Alcoholism - microbiology</subject><subject>Alcoholism - physiopathology</subject><subject>Animals</subject><subject>Anti-Bacterial Agents - adverse effects</subject><subject>Bacteria</subject><subject>Bile Acids and Salts - metabolism</subject><subject>Cecum</subject><subject>Diet</subject><subject>Dietary Supplements - microbiology</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis - immunology</subject><subject>Dysbiosis - metabolism</subject><subject>Ethanol</subject><subject>Ethnicity</subject><subject>Fecal Microbiota Transplantation</subject><subject>Feces</subject><subject>Gastrointestinal Microbiome - physiology</subject><subject>Gene expression</subject><subject>Gram-positive bacteria</subject><subject>Hepatitis</subject><subject>Hepatocytes - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - microbiology</subject><subject>Irritable bowel syndrome</subject><subject>Liver - metabolism</subject><subject>Liver - physiopathology</subject><subject>Liver diseases</subject><subject>Liver Diseases, Alcoholic - immunology</subject><subject>Liver Diseases, Alcoholic - metabolism</subject><subject>Liver Diseases, Alcoholic - microbiology</subject><subject>Liver Diseases, Alcoholic - physiopathology</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Microbiota</subject><subject>Microorganisms</subject><subject>Oats</subject><subject>Permeability</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Review</subject><subject>Small intestine</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LAzEQxYMotlZvnmXBiwdX87H58qCUorVQ8aJ4DLvZ1E3ZbWqyK_S_N6W1VOcyA-_HY94MAOcI3hAi4a2dNwFDJDLKxAHoowzjFELGD_fmHjgJYQ4hJpjKY9AjiGYQEdIH6bDWrnJ14nwy7trkxWrvCuva_C75qFwyCUlbmSjZul09nIKjWV4Hc7btA_D-9Pg2ek6nr-PJaDhNdcZFm5Yccgk15VQXIi8wxdwwIiUsuRZoBgtBOEdlyZjUhGZaU80yBqNAICdUkAG43_guu6IxpTaL1ue1Wnrb5H6lXG7VX2VhK_XpvhXjHJJYA3C1NfDuqzOhVY0N2tR1vjCuCwpjSTNBOVujl__Quev8IsZTODoJLAiWkbreUPE8IXgz2y2DoFr_Qe3_IeIX-wF28O_hyQ8SAIDh</recordid><startdate>20190914</startdate><enddate>20190914</enddate><creator>Meroni, Marica</creator><creator>Longo, Miriam</creator><creator>Dongiovanni, Paola</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9433-3492</orcidid><orcidid>https://orcid.org/0000-0003-4343-7213</orcidid><orcidid>https://orcid.org/0000-0002-4161-4178</orcidid></search><sort><creationdate>20190914</creationdate><title>Alcohol or Gut Microbiota: Who Is the Guilty?</title><author>Meroni, Marica ; Longo, Miriam ; Dongiovanni, Paola</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-d70790c575cb8ab2527e63990d7c81f0b83771dd669c354cc5c6460f0b3073583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alcohol</topic><topic>Alcoholism - 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metabolism</topic><topic>Liver - physiopathology</topic><topic>Liver diseases</topic><topic>Liver Diseases, Alcoholic - immunology</topic><topic>Liver Diseases, Alcoholic - metabolism</topic><topic>Liver Diseases, Alcoholic - microbiology</topic><topic>Liver Diseases, Alcoholic - physiopathology</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Microbiota</topic><topic>Microorganisms</topic><topic>Oats</topic><topic>Permeability</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Review</topic><topic>Small intestine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meroni, Marica</creatorcontrib><creatorcontrib>Longo, Miriam</creatorcontrib><creatorcontrib>Dongiovanni, Paola</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - 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ALD encompasses a broad spectrum of hepatic injuries including asymptomatic steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The susceptibility of alcoholic patients to develop ALD is highly variable and its progression to more advanced stages is strongly influenced by several hits (i.e., amount and duration of alcohol abuse). Among them, the intestinal microbiota and its metabolites have been recently identified as paramount in ALD pathophysiology. Ethanol abuse triggers qualitative and quantitative modifications in intestinal flora taxonomic composition, mucosal inflammation, and intestinal barrier derangement. Intestinal hypermeability results in the translocation of viable pathogenic bacteria, Gram-negative microbial products, and pro-inflammatory luminal metabolites into the bloodstream, further corroborating the alcohol-induced liver damage. 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| subjects | Alcohol Alcoholism - genetics Alcoholism - immunology Alcoholism - microbiology Alcoholism - physiopathology Animals Anti-Bacterial Agents - adverse effects Bacteria Bile Acids and Salts - metabolism Cecum Diet Dietary Supplements - microbiology Dysbacteriosis Dysbiosis - immunology Dysbiosis - metabolism Ethanol Ethnicity Fecal Microbiota Transplantation Feces Gastrointestinal Microbiome - physiology Gene expression Gram-positive bacteria Hepatitis Hepatocytes - metabolism Homeostasis Humans Inflammation Injuries Intestinal microflora Intestine Intestines - microbiology Irritable bowel syndrome Liver - metabolism Liver - physiopathology Liver diseases Liver Diseases, Alcoholic - immunology Liver Diseases, Alcoholic - metabolism Liver Diseases, Alcoholic - microbiology Liver Diseases, Alcoholic - physiopathology Metabolism Metabolites Microbiota Microorganisms Oats Permeability Physiology Proteins Review Small intestine |
| title | Alcohol or Gut Microbiota: Who Is the Guilty? |
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