Bacterial and eukaryotic extracellular vesicles and nonalcoholic fatty liver disease: new players in the gut-liver axis?
The liver and intestine communicate in a bidirectional way through the biliary tract, portal vein, and other components of the gut-liver axis. The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dy...
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Veröffentlicht in: | American journal of physiology: Gastrointestinal and liver physiology 2021-04, Vol.320 (4), p.G485-G495 |
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description | The liver and intestine communicate in a bidirectional way through the biliary tract, portal vein, and other components of the gut-liver axis. The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dysbiosis, participates in the development and progression of several chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD). NAFLD is currently considered the main chronic liver disease worldwide. Dysbiosis contributes to NAFLD development and progression, notably by a greater translocation of pathogen-associated molecular patterns (PAMPs) in the blood. Lipopolysaccharide (LPS) is a PAMP that activates Toll-like receptor 4 (TLR4), induces liver inflammation, and participates in the development of fibrogenesis. LPS can be transported by bacterial extracellular vesicles (EVs). EVs are spherical structures produced by eukaryotic and prokaryotic cells that transfer information to distant cells and may represent new players in NAFLD development and progression. The present review summarizes the role of eukaryotic EVs, either circulating or tissue-derived, in NAFLD features, such as liver inflammation, angiogenesis, and fibrosis. Circulating EV levels are dynamic and correlate with disease stage and severity. However, scarce information is available concerning the involvement of bacterial EVs in liver disease. The present review highlights a potential role of bacterial EVs in insulin resistance and liver inflammation, although the mechanism involved has not been elucidated. In addition, because of their distinct signatures, eukaryotic and prokaryotic EVs may also represent a promising NAFLD diagnostic tool as a "liquid biopsy" in the future. |
doi_str_mv | 10.1152/ajpgi.00362.2020 |
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The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dysbiosis, participates in the development and progression of several chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD). NAFLD is currently considered the main chronic liver disease worldwide. Dysbiosis contributes to NAFLD development and progression, notably by a greater translocation of pathogen-associated molecular patterns (PAMPs) in the blood. Lipopolysaccharide (LPS) is a PAMP that activates Toll-like receptor 4 (TLR4), induces liver inflammation, and participates in the development of fibrogenesis. LPS can be transported by bacterial extracellular vesicles (EVs). EVs are spherical structures produced by eukaryotic and prokaryotic cells that transfer information to distant cells and may represent new players in NAFLD development and progression. The present review summarizes the role of eukaryotic EVs, either circulating or tissue-derived, in NAFLD features, such as liver inflammation, angiogenesis, and fibrosis. Circulating EV levels are dynamic and correlate with disease stage and severity. However, scarce information is available concerning the involvement of bacterial EVs in liver disease. The present review highlights a potential role of bacterial EVs in insulin resistance and liver inflammation, although the mechanism involved has not been elucidated. 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The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dysbiosis, participates in the development and progression of several chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD). NAFLD is currently considered the main chronic liver disease worldwide. Dysbiosis contributes to NAFLD development and progression, notably by a greater translocation of pathogen-associated molecular patterns (PAMPs) in the blood. Lipopolysaccharide (LPS) is a PAMP that activates Toll-like receptor 4 (TLR4), induces liver inflammation, and participates in the development of fibrogenesis. LPS can be transported by bacterial extracellular vesicles (EVs). EVs are spherical structures produced by eukaryotic and prokaryotic cells that transfer information to distant cells and may represent new players in NAFLD development and progression. The present review summarizes the role of eukaryotic EVs, either circulating or tissue-derived, in NAFLD features, such as liver inflammation, angiogenesis, and fibrosis. Circulating EV levels are dynamic and correlate with disease stage and severity. However, scarce information is available concerning the involvement of bacterial EVs in liver disease. The present review highlights a potential role of bacterial EVs in insulin resistance and liver inflammation, although the mechanism involved has not been elucidated. In addition, because of their distinct signatures, eukaryotic and prokaryotic EVs may also represent a promising NAFLD diagnostic tool as a "liquid biopsy" in the future.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacteria - metabolism</subject><subject>Bacterial vesicles</subject><subject>Bile acids</subject><subject>Biliary tract</subject><subject>Biopsy</subject><subject>Digestive system</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis</subject><subject>Extracellular vesicles</subject><subject>Extracellular Vesicles - metabolism</subject><subject>Extracellular Vesicles - microbiology</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>Gastrointestinal Microbiome</subject><subject>Gastrointestinal tract</subject><subject>Host-Pathogen Interactions</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - microbiology</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Liver - metabolism</subject><subject>Liver diseases</subject><subject>Microbiota</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Non-alcoholic Fatty Liver Disease - microbiology</subject><subject>Pathogen-Associated Molecular Pattern Molecules - metabolism</subject><subject>Portal vein</subject><subject>Signal Transduction</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0U1vEzEQBmALgWhauHNClrjQwwZ_28ulKhVQpEhc4Gw53tnGwdkNtjck_x4nKT1wsjR6ZmzPi9AbSuaUSvbBrbcPYU4IV2zOCCPP0KyWWUOl0M_RjNCWN9RIfYEuc14TQiSj9CW64Fxoqjibof0n5wuk4CJ2Q4dh-uXSYSzBY9iX5DzEOEWX8A5y8BHySQ3j4KIfV2OsrnelHHAMO0i4Cxlcho94gD94G90BUsZhwGUF-GEqzVm5fcg3r9CL3sUMrx_PK_Tzy-cfd_fN4vvXb3e3i8YLpkvDeNt72UthmBLKe7EkeslBU9GaTnWmlboXSrJeCy36pXJecUcE54bRDrjgV-j6PHflot2msKn_s6ML9v52YY81wpmpV-kdrfb92W7T-HuCXOwm5OMK3ADjlC0TutXEtIZX-u4_uh6nVNdSlaRGUKWoqYqclU9jzgn6pxdQYo8J2lOC9pSgPSZYW94-Dp6WG-ieGv5Fxv8CzzmW8A</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Villard, Alexandre</creator><creator>Boursier, Jérôme</creator><creator>Andriantsitohaina, Ramaroson</creator><general>American Physiological Society</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>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-6572-4419</orcidid><orcidid>https://orcid.org/0000-0002-4770-3585</orcidid></search><sort><creationdate>20210401</creationdate><title>Bacterial and eukaryotic extracellular vesicles and nonalcoholic fatty liver disease: new players in the gut-liver axis?</title><author>Villard, Alexandre ; Boursier, Jérôme ; Andriantsitohaina, Ramaroson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-239fc5f5482646cc4b07b3e71498d6d8957f4652f7474fb6ac63a0433821de343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Bacteria - metabolism</topic><topic>Bacterial vesicles</topic><topic>Bile acids</topic><topic>Biliary tract</topic><topic>Biopsy</topic><topic>Digestive system</topic><topic>Dysbacteriosis</topic><topic>Dysbiosis</topic><topic>Extracellular vesicles</topic><topic>Extracellular Vesicles - metabolism</topic><topic>Extracellular Vesicles - microbiology</topic><topic>Fatty liver</topic><topic>Fibrosis</topic><topic>Gastrointestinal Microbiome</topic><topic>Gastrointestinal tract</topic><topic>Host-Pathogen Interactions</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Intestines - microbiology</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Liver - metabolism</topic><topic>Liver diseases</topic><topic>Microbiota</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Non-alcoholic Fatty Liver Disease - microbiology</topic><topic>Pathogen-Associated Molecular Pattern Molecules - metabolism</topic><topic>Portal vein</topic><topic>Signal Transduction</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Villard, Alexandre</creatorcontrib><creatorcontrib>Boursier, Jérôme</creatorcontrib><creatorcontrib>Andriantsitohaina, Ramaroson</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Villard, Alexandre</au><au>Boursier, Jérôme</au><au>Andriantsitohaina, Ramaroson</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bacterial and eukaryotic extracellular vesicles and nonalcoholic fatty liver disease: new players in the gut-liver axis?</atitle><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>320</volume><issue>4</issue><spage>G485</spage><epage>G495</epage><pages>G485-G495</pages><issn>0193-1857</issn><eissn>1522-1547</eissn><abstract>The liver and intestine communicate in a bidirectional way through the biliary tract, portal vein, and other components of the gut-liver axis. The gut microbiota is one of the major contributors to the production of several proteins and bile acids. Imbalance in the gut bacterial community, called dysbiosis, participates in the development and progression of several chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD). NAFLD is currently considered the main chronic liver disease worldwide. Dysbiosis contributes to NAFLD development and progression, notably by a greater translocation of pathogen-associated molecular patterns (PAMPs) in the blood. Lipopolysaccharide (LPS) is a PAMP that activates Toll-like receptor 4 (TLR4), induces liver inflammation, and participates in the development of fibrogenesis. LPS can be transported by bacterial extracellular vesicles (EVs). EVs are spherical structures produced by eukaryotic and prokaryotic cells that transfer information to distant cells and may represent new players in NAFLD development and progression. The present review summarizes the role of eukaryotic EVs, either circulating or tissue-derived, in NAFLD features, such as liver inflammation, angiogenesis, and fibrosis. Circulating EV levels are dynamic and correlate with disease stage and severity. However, scarce information is available concerning the involvement of bacterial EVs in liver disease. The present review highlights a potential role of bacterial EVs in insulin resistance and liver inflammation, although the mechanism involved has not been elucidated. In addition, because of their distinct signatures, eukaryotic and prokaryotic EVs may also represent a promising NAFLD diagnostic tool as a "liquid biopsy" in the future.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>33471632</pmid><doi>10.1152/ajpgi.00362.2020</doi><orcidid>https://orcid.org/0000-0002-6572-4419</orcidid><orcidid>https://orcid.org/0000-0002-4770-3585</orcidid></addata></record> |
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subjects | Angiogenesis Animals Bacteria Bacteria - metabolism Bacterial vesicles Bile acids Biliary tract Biopsy Digestive system Dysbacteriosis Dysbiosis Extracellular vesicles Extracellular Vesicles - metabolism Extracellular Vesicles - microbiology Fatty liver Fibrosis Gastrointestinal Microbiome Gastrointestinal tract Host-Pathogen Interactions Humans Inflammation Insulin Insulin resistance Intestinal microflora Intestine Intestines - microbiology Life Sciences Lipopolysaccharides Liver - metabolism Liver diseases Microbiota Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - microbiology Pathogen-Associated Molecular Pattern Molecules - metabolism Portal vein Signal Transduction TLR4 protein Toll-like receptors |
title | Bacterial and eukaryotic extracellular vesicles and nonalcoholic fatty liver disease: new players in the gut-liver axis? |
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