Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis
Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirr...
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| Veröffentlicht in: | PloS one 2017-03, Vol.12 (3), p.e0172575-e0172575 |
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| creator | Cannito, Stefania Morello, Elisabetta Bocca, Claudia Foglia, Beatrice Benetti, Elisa Novo, Erica Chiazza, Fausto Rogazzo, Mara Fantozzi, Roberto Povero, Davide Sutti, Salvatore Bugianesi, Elisabetta Feldstein, Ariel E Albano, Emanuele Collino, Massimo Parola, Maurizio |
| description | Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response. |
| doi_str_mv | 10.1371/journal.pone.0172575 |
| format | Article |
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NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0172575</identifier><identifier>PMID: 28249038</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; Autoimmune diseases ; Biology and Life Sciences ; Body weight ; Care and treatment ; Caspase ; Caspase 1 - metabolism ; Caspase-1 ; Cell activation ; Cell-Derived Microparticles - metabolism ; Cirrhosis ; Complex formation ; Complications and side effects ; Cytokines ; Diabetes ; Diabetes mellitus ; Diabetics ; Diagnosis ; Fatty acids ; Fatty liver ; Fibrosis ; Gastroenterology ; Health sciences ; Hepatitis ; Hypoxia ; Inflammasomes ; Inflammasomes - metabolism ; Inflammation ; Inflammatory response ; Interdisciplinary aspects ; Interleukin 1 ; Interleukin-1 - metabolism ; Internalization ; Ligands ; Lipids ; Liver ; Liver - metabolism ; Liver - pathology ; Liver cirrhosis ; Liver diseases ; Macrophages ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Medicine and Health Sciences ; Metabolic disorders ; Metabolic syndrome ; Mice ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Non-alcoholic Fatty Liver Disease - metabolism ; Non-alcoholic Fatty Liver Disease - pathology ; Overweight ; Pediatrics ; Polyclonal antibodies ; Protein Precursors - metabolism ; Research and Analysis Methods ; Risk factors ; Rodents</subject><ispartof>PloS one, 2017-03, Vol.12 (3), p.e0172575-e0172575</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Cannito et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Cannito et al 2017 Cannito et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-5220a1db76521b41dc24bfa4f6e2d194407f6180e4996a7cb3014e23f3a7eba13</citedby><cites>FETCH-LOGICAL-c791t-5220a1db76521b41dc24bfa4f6e2d194407f6180e4996a7cb3014e23f3a7eba13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331985/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331985/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28249038$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cannito, Stefania</creatorcontrib><creatorcontrib>Morello, Elisabetta</creatorcontrib><creatorcontrib>Bocca, Claudia</creatorcontrib><creatorcontrib>Foglia, Beatrice</creatorcontrib><creatorcontrib>Benetti, Elisa</creatorcontrib><creatorcontrib>Novo, Erica</creatorcontrib><creatorcontrib>Chiazza, Fausto</creatorcontrib><creatorcontrib>Rogazzo, Mara</creatorcontrib><creatorcontrib>Fantozzi, Roberto</creatorcontrib><creatorcontrib>Povero, Davide</creatorcontrib><creatorcontrib>Sutti, Salvatore</creatorcontrib><creatorcontrib>Bugianesi, Elisabetta</creatorcontrib><creatorcontrib>Feldstein, Ariel E</creatorcontrib><creatorcontrib>Albano, Emanuele</creatorcontrib><creatorcontrib>Collino, Massimo</creatorcontrib><creatorcontrib>Parola, Maurizio</creatorcontrib><title>Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Autoimmune diseases</subject><subject>Biology and Life Sciences</subject><subject>Body weight</subject><subject>Care and treatment</subject><subject>Caspase</subject><subject>Caspase 1 - metabolism</subject><subject>Caspase-1</subject><subject>Cell activation</subject><subject>Cell-Derived Microparticles - metabolism</subject><subject>Cirrhosis</subject><subject>Complex formation</subject><subject>Complications and side effects</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetics</subject><subject>Diagnosis</subject><subject>Fatty acids</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>Gastroenterology</subject><subject>Health sciences</subject><subject>Hepatitis</subject><subject>Hypoxia</subject><subject>Inflammasomes</subject><subject>Inflammasomes - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cannito, Stefania</au><au>Morello, Elisabetta</au><au>Bocca, Claudia</au><au>Foglia, Beatrice</au><au>Benetti, Elisa</au><au>Novo, Erica</au><au>Chiazza, Fausto</au><au>Rogazzo, Mara</au><au>Fantozzi, Roberto</au><au>Povero, Davide</au><au>Sutti, Salvatore</au><au>Bugianesi, Elisabetta</au><au>Feldstein, Ariel E</au><au>Albano, Emanuele</au><au>Collino, Massimo</au><au>Parola, Maurizio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>12</volume><issue>3</issue><spage>e0172575</spage><epage>e0172575</epage><pages>e0172575-e0172575</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1β. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28249038</pmid><doi>10.1371/journal.pone.0172575</doi><tpages>e0172575</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-03, Vol.12 (3), p.e0172575-e0172575 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1873345191 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Animals Apoptosis Autoimmune diseases Biology and Life Sciences Body weight Care and treatment Caspase Caspase 1 - metabolism Caspase-1 Cell activation Cell-Derived Microparticles - metabolism Cirrhosis Complex formation Complications and side effects Cytokines Diabetes Diabetes mellitus Diabetics Diagnosis Fatty acids Fatty liver Fibrosis Gastroenterology Health sciences Hepatitis Hypoxia Inflammasomes Inflammasomes - metabolism Inflammation Inflammatory response Interdisciplinary aspects Interleukin 1 Interleukin-1 - metabolism Internalization Ligands Lipids Liver Liver - metabolism Liver - pathology Liver cirrhosis Liver diseases Macrophages Macrophages - metabolism Macrophages - pathology Male Medicine and Health Sciences Metabolic disorders Metabolic syndrome Mice NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Overweight Pediatrics Polyclonal antibodies Protein Precursors - metabolism Research and Analysis Methods Risk factors Rodents |
| title | Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis |
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