The effects of insulin on the inflammatory activity of BV2 microglia
Microglia are the macrophages of the central nervous system (CNS), which function to monitor and maintain homeostasis. Microglial activation occurs after CNS injury, infection or disease. Prolonged microglial activation is detrimental to the CNS as they produce nitric oxide (NO), reactive oxygen spe...
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| description | Microglia are the macrophages of the central nervous system (CNS), which function to monitor and maintain homeostasis. Microglial activation occurs after CNS injury, infection or disease. Prolonged microglial activation is detrimental to the CNS as they produce nitric oxide (NO), reactive oxygen species (ROS) and pro-inflammatory cytokines, resulting in neuronal cell dysfunction and death. Microglial activation is implicated in the neurological deficits following traumatic brain injury (TBI) and Alzheimer's disease. Intranasal insulin administration is a promising treatment of Alzheimer's disease and TBI. However, the exact effect of insulin on microglia is currently unclear. The goal of this study was therefore to examine the effect of insulin administration on activated microglia. The microglial cell line BV2 were exposed to a pro-inflammatory stimulus, lipopolysaccharide (LPS), followed by insulin administration. Outcome measures were conducted at 24 hours after treatment. In vitro assays quantified NO and ROS production. Western blot, immunocytochemistry and phagocytosis assay further examined the effect of insulin on microglial activity. Insulin treatment significantly reduced NO, ROS and TNFα production and increased phagocytic activity. Insulin treatment also significantly reduced iNOS expression, but had no significant effect on any other M1 or M2 macrophage polarization marker examined. These data suggest that insulin has very specific effects to reduce pro-inflammatory or chemoattractant properties of microglia, and this may be one mechanism by which insulin has beneficial effects in CNS injury or neurodegenerative conditions. |
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Microglial activation occurs after CNS injury, infection or disease. Prolonged microglial activation is detrimental to the CNS as they produce nitric oxide (NO), reactive oxygen species (ROS) and pro-inflammatory cytokines, resulting in neuronal cell dysfunction and death. Microglial activation is implicated in the neurological deficits following traumatic brain injury (TBI) and Alzheimer's disease. Intranasal insulin administration is a promising treatment of Alzheimer's disease and TBI. However, the exact effect of insulin on microglia is currently unclear. The goal of this study was therefore to examine the effect of insulin administration on activated microglia. The microglial cell line BV2 were exposed to a pro-inflammatory stimulus, lipopolysaccharide (LPS), followed by insulin administration. Outcome measures were conducted at 24 hours after treatment. In vitro assays quantified NO and ROS production. Western blot, immunocytochemistry and phagocytosis assay further examined the effect of insulin on microglial activity. Insulin treatment significantly reduced NO, ROS and TNFα production and increased phagocytic activity. Insulin treatment also significantly reduced iNOS expression, but had no significant effect on any other M1 or M2 macrophage polarization marker examined. These data suggest that insulin has very specific effects to reduce pro-inflammatory or chemoattractant properties of microglia, and this may be one mechanism by which insulin has beneficial effects in CNS injury or neurodegenerative conditions.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0201878</identifier><identifier>PMID: 30148836</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Alzheimer's disease ; Anatomy & physiology ; Animal cognition ; Animals ; Apoptosis ; beta-N-Acetylhexosaminidases - metabolism ; Biology and Life Sciences ; Brain ; Brain injuries ; Care and treatment ; Cell death ; Cell Line ; Central nervous system ; Cytokines ; Diabetes ; Gene expression ; Genetic aspects ; Head injuries ; Health aspects ; Health sciences ; Homeostasis ; Immunocytochemistry ; Inflammation ; Inflammation - metabolism ; Insulin ; Insulin - administration & dosage ; Insulin - metabolism ; Lectins - metabolism ; Lectins, C-Type - metabolism ; Lipopolysaccharides ; Macrophages ; Mannose Receptor ; Mannose-Binding Lectins - metabolism ; Medical treatment ; Medicine and Health Sciences ; Memory ; Mice ; Microglia ; Microglia - immunology ; Microglia - pathology ; Neurological diseases ; Neurosciences ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric-oxide synthase ; Oxidative stress ; Oxygen ; Phagocytes ; Phagocytosis ; Phagocytosis - physiology ; Physiological aspects ; Physiology ; Properties ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptors, Cell Surface - metabolism ; Risk factors ; Rodents ; TNF inhibitors ; Traumatic brain injury ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2018-08, Vol.13 (8), p.e0201878-e0201878</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication: https://creativecommons.org/publicdomain/zero/1.0/ (the “License”). 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Microglial activation occurs after CNS injury, infection or disease. Prolonged microglial activation is detrimental to the CNS as they produce nitric oxide (NO), reactive oxygen species (ROS) and pro-inflammatory cytokines, resulting in neuronal cell dysfunction and death. Microglial activation is implicated in the neurological deficits following traumatic brain injury (TBI) and Alzheimer's disease. Intranasal insulin administration is a promising treatment of Alzheimer's disease and TBI. However, the exact effect of insulin on microglia is currently unclear. The goal of this study was therefore to examine the effect of insulin administration on activated microglia. The microglial cell line BV2 were exposed to a pro-inflammatory stimulus, lipopolysaccharide (LPS), followed by insulin administration. Outcome measures were conducted at 24 hours after treatment. In vitro assays quantified NO and ROS production. Western blot, immunocytochemistry and phagocytosis assay further examined the effect of insulin on microglial activity. Insulin treatment significantly reduced NO, ROS and TNFα production and increased phagocytic activity. Insulin treatment also significantly reduced iNOS expression, but had no significant effect on any other M1 or M2 macrophage polarization marker examined. 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metabolism</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>TNF inhibitors</subject><subject>Traumatic brain injury</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkt9v0zAQxyMEYqPwHyCIhITgocWOk9h-QRrjV6VJk2Ds1bo4l9aVE5fYmeh_j7tmU4P2gPxgy_7c93x33yR5ScmCMk4_bNzQd2AXW9fhgmSECi4eJadUsmxeZoQ9PjqfJM-83xBSMFGWT5MTRmguBCtPk89Xa0yxaVAHn7omNZ0frOlS16UhvpiusdC2EFy_S0EHc2PCbs99us7S1ujerayB58mTBqzHF-M-S359_XJ1_n1-cflteX52Mde8EGFeoqglCMEpENmUGiklOSU10YhacykE1AC6JlWVYUYkF1wLKTkyXWYMGjZLXh90t9Z5NTbAq4jmrBAlF5FYHojawUZte9NCv1MOjLq9cP1KQR-MtqiqrGINr3NWapYXVQWUVjnhWNEsJ7KootbHMdtQtVhr7EIPdiI6fenMWq3cjSr3dcUfz5J3o0Dvfg_og2qN12gtdOiG238XRU4FkxF98w_6cHUjtYJYQJyNi3n1XlSdFQWVmSwYi9TiASquGuPEolsaE-8nAe8nAZEJ-CesYPBeLX_--H_28nrKvj1i1wg2rL2zQzCu81MwP4DRT9732Nw3mRK1N_tdN9Te7Go0ewx7dTyg-6A7d7O_rFz4kQ</recordid><startdate>20180827</startdate><enddate>20180827</enddate><creator>Brabazon, Fiona</creator><creator>Bermudez, Sara</creator><creator>Shaughness, Michael</creator><creator>Khayrullina, Guzal</creator><creator>Byrnes, Kimberly R</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7501-7734</orcidid></search><sort><creationdate>20180827</creationdate><title>The effects of insulin on the inflammatory activity of BV2 microglia</title><author>Brabazon, Fiona ; Bermudez, Sara ; Shaughness, Michael ; Khayrullina, Guzal ; Byrnes, Kimberly R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-6e8d9a8871a09f6ce110410d0ceecc7988adaacd0bb2e209787c8997e3c623af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Alzheimer's disease</topic><topic>Anatomy & physiology</topic><topic>Animal cognition</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>beta-N-Acetylhexosaminidases - metabolism</topic><topic>Biology and Life Sciences</topic><topic>Brain</topic><topic>Brain injuries</topic><topic>Care and treatment</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>Central nervous system</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Head injuries</topic><topic>Health aspects</topic><topic>Health sciences</topic><topic>Homeostasis</topic><topic>Immunocytochemistry</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - metabolism</topic><topic>Lectins - metabolism</topic><topic>Lectins, C-Type - metabolism</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Mannose Receptor</topic><topic>Mannose-Binding Lectins - metabolism</topic><topic>Medical treatment</topic><topic>Medicine and Health Sciences</topic><topic>Memory</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microglia - 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Microglial activation occurs after CNS injury, infection or disease. Prolonged microglial activation is detrimental to the CNS as they produce nitric oxide (NO), reactive oxygen species (ROS) and pro-inflammatory cytokines, resulting in neuronal cell dysfunction and death. Microglial activation is implicated in the neurological deficits following traumatic brain injury (TBI) and Alzheimer's disease. Intranasal insulin administration is a promising treatment of Alzheimer's disease and TBI. However, the exact effect of insulin on microglia is currently unclear. The goal of this study was therefore to examine the effect of insulin administration on activated microglia. The microglial cell line BV2 were exposed to a pro-inflammatory stimulus, lipopolysaccharide (LPS), followed by insulin administration. Outcome measures were conducted at 24 hours after treatment. In vitro assays quantified NO and ROS production. Western blot, immunocytochemistry and phagocytosis assay further examined the effect of insulin on microglial activity. Insulin treatment significantly reduced NO, ROS and TNFα production and increased phagocytic activity. Insulin treatment also significantly reduced iNOS expression, but had no significant effect on any other M1 or M2 macrophage polarization marker examined. These data suggest that insulin has very specific effects to reduce pro-inflammatory or chemoattractant properties of microglia, and this may be one mechanism by which insulin has beneficial effects in CNS injury or neurodegenerative conditions.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>30148836</pmid><doi>10.1371/journal.pone.0201878</doi><tpages>e0201878</tpages><orcidid>https://orcid.org/0000-0002-7501-7734</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Activation Alzheimer's disease Anatomy & physiology Animal cognition Animals Apoptosis beta-N-Acetylhexosaminidases - metabolism Biology and Life Sciences Brain Brain injuries Care and treatment Cell death Cell Line Central nervous system Cytokines Diabetes Gene expression Genetic aspects Head injuries Health aspects Health sciences Homeostasis Immunocytochemistry Inflammation Inflammation - metabolism Insulin Insulin - administration & dosage Insulin - metabolism Lectins - metabolism Lectins, C-Type - metabolism Lipopolysaccharides Macrophages Mannose Receptor Mannose-Binding Lectins - metabolism Medical treatment Medicine and Health Sciences Memory Mice Microglia Microglia - immunology Microglia - pathology Neurological diseases Neurosciences Nitric oxide Nitric Oxide - metabolism Nitric-oxide synthase Oxidative stress Oxygen Phagocytes Phagocytosis Phagocytosis - physiology Physiological aspects Physiology Properties Proteins Proto-Oncogene Proteins c-akt - metabolism Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Cell Surface - metabolism Risk factors Rodents TNF inhibitors Traumatic brain injury Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | The effects of insulin on the inflammatory activity of BV2 microglia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T02%3A04%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20effects%20of%20insulin%20on%20the%20inflammatory%20activity%20of%20BV2%20microglia&rft.jtitle=PloS%20one&rft.au=Brabazon,%20Fiona&rft.date=2018-08-27&rft.volume=13&rft.issue=8&rft.spage=e0201878&rft.epage=e0201878&rft.pages=e0201878-e0201878&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0201878&rft_dat=%3Cgale_plos_%3EA551929533%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2094358678&rft_id=info:pmid/30148836&rft_galeid=A551929533&rft_doaj_id=oai_doaj_org_article_b2b3f7d436c345bba11b407eb124095b&rfr_iscdi=true |