Cytokines, chemokines, and cytokine receptors in human microglia
Identifieur interne : 002993 ( Main/Corpus ); précédent : 002992; suivant : 002994Cytokines, chemokines, and cytokine receptors in human microglia
Auteurs : Yong B. Lee ; Atsushi Nagai ; Seung U. KimSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2002-07-01.
English descriptors
- KwdEn :
Abstract
Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma. © 2002 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.10253
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Lee</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</mods:affiliation></affiliation></author><author><name sortKey="Nagai, Atsushi" sort="Nagai, Atsushi" uniqKey="Nagai A" first="Atsushi" last="Nagai">Atsushi Nagai</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Current Address: Department of Medicine, Shimane Medical University, Izumo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. 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Lee</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</mods:affiliation></affiliation></author><author><name sortKey="Nagai, Atsushi" sort="Nagai, Atsushi" uniqKey="Nagai A" first="Atsushi" last="Nagai">Atsushi Nagai</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Current Address: Department of Medicine, Shimane Medical University, Izumo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. 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Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma. © 2002 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yong B. Lee</name><affiliations><json:string>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</json:string><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</json:string></affiliations></json:item><json:item><name>Atsushi Nagai</name><affiliations><json:string>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</json:string><json:string>Current Address: Department of Medicine, Shimane Medical University, Izumo, Japan</json:string></affiliations></json:item><json:item><name>Seung U. 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Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). 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Lee and Atsushi Nagai contributed equally to the work.</note><affiliation>Yong B. Lee and Atsushi Nagai contributed equally to the work.</affiliation><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</affiliation></author><author><persName><forename type="first">Atsushi</forename><surname>Nagai</surname></persName><note type="biography">Yong B. Lee and Atsushi Nagai contributed equally to the work.</note><affiliation>Yong B. Lee and Atsushi Nagai contributed equally to the work.</affiliation><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Current Address: Department of Medicine, Shimane Medical University, Izumo, Japan</affiliation></author><author><persName><forename type="first">Seung U.</forename><surname>Kim</surname></persName><note type="correspondence"><p>Correspondence: Brain Disease Research Center, Ajou University Scool of Medicine, 5 San, Wonchon‐Dong, Suwon, Korea 442‐721</p></note><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</affiliation></author></analytic><monogr><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="pISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><idno type="DOI">10.1002/(ISSN)1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-07-01"></date><biblScope unit="volume">69</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="94">94</biblScope><biblScope unit="page" to="103">103</biblScope></imprint></monogr><idno type="istex">59767AA942795D3BB001834C159997CF1068823B</idno><idno type="DOI">10.1002/jnr.10253</idno><idno type="ArticleID">JNR10253</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma. © 2002 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>amyloid β peptides</term></item><item><term>cytokines</term></item><item><term>cytokine receptors</term></item><item><term>chemokines</term></item><item><term>human microglia</term></item><item><term>lipopolysaccharide</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-12-18">Received</change><change when="2002-03-06">Registration</change><change when="2002-07-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/59767AA942795D3BB001834C159997CF1068823B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4547</doi><issn type="print">0360-4012</issn><issn type="electronic">1097-4547</issn><idGroup><id type="product" value="JNR"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF NEUROSCIENCE RESEARCH">Journal of Neuroscience Research</title><title type="short">J. 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Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma. © 2002 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Yong B. Lee and Atsushi Nagai contributed equally to the work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cytokines, chemokines, and cytokine receptors in human microglia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cytokines and Cytokine Receptors in Human Microglia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cytokines, chemokines, and cytokine receptors in human microglia</title></titleInfo><name type="personal"><namePart type="given">Yong B.</namePart><namePart type="family">Lee</namePart><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</affiliation><description>Yong B. Lee and Atsushi Nagai contributed equally to the work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Atsushi</namePart><namePart type="family">Nagai</namePart><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Current Address: Department of Medicine, Shimane Medical University, Izumo, Japan</affiliation><description>Yong B. Lee and Atsushi Nagai contributed equally to the work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seung U.</namePart><namePart type="family">Kim</namePart><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada</affiliation><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</affiliation><description>Correspondence: Brain Disease Research Center, Ajou University Scool of Medicine, 5 San, Wonchon‐Dong, Suwon, Korea 442‐721</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-07-01</dateIssued><dateCaptured encoding="w3cdtf">2001-12-18</dateCaptured><dateValid encoding="w3cdtf">2002-03-06</dateValid><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">37</extent><extent unit="words">5292</extent></physicalDescription><abstract lang="en">Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. Human microglial cells exhibited cell type‐specific antigens for macrophage‐microglia lineage cells including CD11b (Mac‐1), CD68, B7‐2 (CD86), HLA‐ABC, HLA‐DR and ricinus communis aggulutinin lectin‐1 (RCA‐1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin‐ 1β (IL‐1β) ‐6, ‐8, ‐10, ‐12, ‐15, tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1α (MIP‐1α), MIP‐1β, and monocyte chemoattractant protein‐1 (MCP‐1), while treatment with lipopolysaccharide (LPS) or amyloid β peptides (Aβ) led to increased expression of mRNA levels of IL‐8, IL‐10, IL‐12, TNF‐α, MIP‐1α, MIP‐1β, and MCP‐1. Human microglia, in addition, expressed mRNA transcripts for IL‐1RI, IL‐1RII, IL‐5R, IL‐6R, IL‐8R, IL‐9R, IL‐10R, IL‐12R, IL‐13R, and IL‐15R. Enzyme‐linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL‐1β, IL‐8, TNF‐α, and MIP‐1α in human microglia following treatment with LPS or Aβ. Increased TNF‐α release from human microglia following LPS treatment was completely inhibited with IL‐10 pretreatment, but not with IL‐6, IL‐9, IL‐12, IL‐13, or transforming growth factor‐β (TGF‐β). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma. © 2002 Wiley‐Liss, Inc.</abstract><note type="funding">Canadian Myelin Research Initiative</note><note type="funding">KOSEF/BDRC Ajou University</note><subject lang="en"><genre>Keywords</genre><topic>amyloid β peptides</topic><topic>cytokines</topic><topic>cytokine receptors</topic><topic>chemokines</topic><topic>human microglia</topic><topic>lipopolysaccharide</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. Res.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0360-4012</identifier><identifier type="eISSN">1097-4547</identifier><identifier type="DOI">10.1002/(ISSN)1097-4547</identifier><identifier type="PublisherID">JNR</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>69</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>94</start><end>103</end><total>10</total></extent></part></relatedItem><identifier type="istex">59767AA942795D3BB001834C159997CF1068823B</identifier><identifier type="DOI">10.1002/jnr.10253</identifier><identifier type="ArticleID">JNR10253</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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