Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro
We have previously developed and characterized isolated microglia and astrocyte cultures from rapid (
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| Veröffentlicht in: | Glia 2001-07, Vol.35 (1), p.72-79 |
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| creator | Lue, Lih-Fen Rydel, Russell Brigham, Elizabeth F. Yang, Li-Bang Hampel, Harald Murphy Jr, Greer M. Brachova, Libuse Yan, Shi-Du Walker, Douglas G. Shen, Yong Rogers, Joseph |
| description | We have previously developed and characterized isolated microglia and astrocyte cultures from rapid ( |
| doi_str_mv | 10.1002/glia.1072 |
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In the present study, we evaluate the inflammatory repertoire of AD and ND microglia cultured from white matter (corpus callosum) and gray matter (superior frontal gyrus) with respect to three major proinflammatory cytokines, three chemokines, a classical pathway complement component, a scavenger cell growth factor, and a reactive nitrogen intermediate. Significant, dose‐dependent increases in the production of pro‐interleukin‐1β (pro‐IL‐1β), interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), monocyte chemoattractant protein‐1 (MCP‐1), macrophage inflammatory peptide‐1α (MIP‐1α), IL‐8, and macrophage colony‐stimulating factor (M‐CSF) were observed after exposure to pre‐aggregated amyloid β peptide (1–42) (Aβ1–42). Across constitutive and Aβ‐stimulated conditions, secretion of complement component C1q, a reactive nitrogen intermediate, and M‐CSF was significantly higher in AD compared with ND microglia. Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators. GLIA 35:72–79, 2001. © 2001 Wiley‐Liss, Inc.</description><identifier>ISSN: 0894-1491</identifier><identifier>EISSN: 1098-1136</identifier><identifier>DOI: 10.1002/glia.1072</identifier><identifier>PMID: 11424194</identifier><identifier>CODEN: GLIAEJ</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Aged ; Aged, 80 and over ; Aging - immunology ; Aging - metabolism ; Aging - pathology ; Alzheimer Disease - immunology ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Amyloid beta-Peptides - pharmacology ; Biological and medical sciences ; Biomarkers - analysis ; Brain - immunology ; Brain - metabolism ; Brain - physiopathology ; cell culture ; Cells, Cultured - drug effects ; Cells, Cultured - immunology ; Cells, Cultured - metabolism ; chemokines ; Chemokines - biosynthesis ; complement ; Complement C1q - biosynthesis ; Complement C1q - drug effects ; Corpus Callosum - immunology ; Corpus Callosum - metabolism ; Corpus Callosum - physiopathology ; cytokines ; Cytokines - biosynthesis ; Cytokines - drug effects ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Encephalitis - immunology ; Encephalitis - metabolism ; Encephalitis - physiopathology ; Female ; Frontal Lobe - immunology ; Frontal Lobe - metabolism ; Frontal Lobe - physiopathology ; glia ; Humans ; inflammation ; Male ; Medical sciences ; Microglia - drug effects ; Microglia - immunology ; Microglia - metabolism ; Neurology ; Nitrites - metabolism ; Peptide Fragments - pharmacology</subject><ispartof>Glia, 2001-07, Vol.35 (1), p.72-79</ispartof><rights>Copyright © 2001 Wiley‐Liss, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2001 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4852-ebdf98041549fb65085cab3ba53599dd49135f126886a90d1d785e709672def53</citedby><cites>FETCH-LOGICAL-c4852-ebdf98041549fb65085cab3ba53599dd49135f126886a90d1d785e709672def53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fglia.1072$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fglia.1072$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1046952$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11424194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lue, Lih-Fen</creatorcontrib><creatorcontrib>Rydel, Russell</creatorcontrib><creatorcontrib>Brigham, Elizabeth F.</creatorcontrib><creatorcontrib>Yang, Li-Bang</creatorcontrib><creatorcontrib>Hampel, Harald</creatorcontrib><creatorcontrib>Murphy Jr, Greer M.</creatorcontrib><creatorcontrib>Brachova, Libuse</creatorcontrib><creatorcontrib>Yan, Shi-Du</creatorcontrib><creatorcontrib>Walker, Douglas G.</creatorcontrib><creatorcontrib>Shen, Yong</creatorcontrib><creatorcontrib>Rogers, Joseph</creatorcontrib><title>Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro</title><title>Glia</title><addtitle>Glia</addtitle><description>We have previously developed and characterized isolated microglia and astrocyte cultures from rapid (<4 h) brain autopsies of Alzheimer's disease (AD) and nondemented elderly control (ND) patients. In the present study, we evaluate the inflammatory repertoire of AD and ND microglia cultured from white matter (corpus callosum) and gray matter (superior frontal gyrus) with respect to three major proinflammatory cytokines, three chemokines, a classical pathway complement component, a scavenger cell growth factor, and a reactive nitrogen intermediate. Significant, dose‐dependent increases in the production of pro‐interleukin‐1β (pro‐IL‐1β), interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), monocyte chemoattractant protein‐1 (MCP‐1), macrophage inflammatory peptide‐1α (MIP‐1α), IL‐8, and macrophage colony‐stimulating factor (M‐CSF) were observed after exposure to pre‐aggregated amyloid β peptide (1–42) (Aβ1–42). Across constitutive and Aβ‐stimulated conditions, secretion of complement component C1q, a reactive nitrogen intermediate, and M‐CSF was significantly higher in AD compared with ND microglia. Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators. GLIA 35:72–79, 2001. © 2001 Wiley‐Liss, Inc.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - immunology</subject><subject>Aging - metabolism</subject><subject>Aging - pathology</subject><subject>Alzheimer Disease - immunology</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Brain - immunology</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>cell culture</subject><subject>Cells, Cultured - drug effects</subject><subject>Cells, Cultured - immunology</subject><subject>Cells, Cultured - metabolism</subject><subject>chemokines</subject><subject>Chemokines - biosynthesis</subject><subject>complement</subject><subject>Complement C1q - biosynthesis</subject><subject>Complement C1q - drug effects</subject><subject>Corpus Callosum - immunology</subject><subject>Corpus Callosum - metabolism</subject><subject>Corpus Callosum - physiopathology</subject><subject>cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - drug effects</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Encephalitis - immunology</subject><subject>Encephalitis - metabolism</subject><subject>Encephalitis - physiopathology</subject><subject>Female</subject><subject>Frontal Lobe - immunology</subject><subject>Frontal Lobe - metabolism</subject><subject>Frontal Lobe - physiopathology</subject><subject>glia</subject><subject>Humans</subject><subject>inflammation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microglia - drug effects</subject><subject>Microglia - immunology</subject><subject>Microglia - metabolism</subject><subject>Neurology</subject><subject>Nitrites - metabolism</subject><subject>Peptide Fragments - pharmacology</subject><issn>0894-1491</issn><issn>1098-1136</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE9v1DAQxa0K1G5LD3wB5AOi4hBqJ_G_46rAsmKBC6jqyXLicWtwksXOAsunx9FGLRfEaWak37x58xB6SskrSkh5eRu8yZ0oj9CCEiULSiv-CC2IVHVBa0VP0GlKXwmheRDH6CTXsqaqXqCbde-C6TozDnGPI2whjoOPgAeHl-H3HfgO4kXC1icwCbDpLe6H3kIH_QgWQ7AQwx53vo3D5AP7Hv_wYxyeoMfOhATncz1DX96--Xz1rth8Wq2vlpuirSUrC2isU5LUlNXKNZwRyVrTVI1hFVPK2uy-Yo6WXEpuFLHUCslAEMVFacGx6gy9OOhu4_B9B2nUnU8thGB6GHZJZ5Qxwch_QSopl6ziGXx5APNLKUVweht9Z-JeU6KnwPX0qJ4Cz-yzWXTXdGAfyDnhDDyfAZNaE1w0fevTX4o1V2zSuTxgP32A_b8P6tVmvZwvF4cNn0b4db9h4jfNRSWYvv640ur1e8bFh2stqj__wKYY</recordid><startdate>200107</startdate><enddate>200107</enddate><creator>Lue, Lih-Fen</creator><creator>Rydel, Russell</creator><creator>Brigham, Elizabeth F.</creator><creator>Yang, Li-Bang</creator><creator>Hampel, Harald</creator><creator>Murphy Jr, Greer M.</creator><creator>Brachova, Libuse</creator><creator>Yan, Shi-Du</creator><creator>Walker, Douglas G.</creator><creator>Shen, Yong</creator><creator>Rogers, Joseph</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>200107</creationdate><title>Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro</title><author>Lue, Lih-Fen ; Rydel, Russell ; Brigham, Elizabeth F. ; Yang, Li-Bang ; Hampel, Harald ; Murphy Jr, Greer M. ; Brachova, Libuse ; Yan, Shi-Du ; Walker, Douglas G. ; Shen, Yong ; Rogers, Joseph</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4852-ebdf98041549fb65085cab3ba53599dd49135f126886a90d1d785e709672def53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - immunology</topic><topic>Aging - metabolism</topic><topic>Aging - pathology</topic><topic>Alzheimer Disease - immunology</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Brain - immunology</topic><topic>Brain - metabolism</topic><topic>Brain - physiopathology</topic><topic>cell culture</topic><topic>Cells, Cultured - drug effects</topic><topic>Cells, Cultured - immunology</topic><topic>Cells, Cultured - metabolism</topic><topic>chemokines</topic><topic>Chemokines - biosynthesis</topic><topic>complement</topic><topic>Complement C1q - biosynthesis</topic><topic>Complement C1q - drug effects</topic><topic>Corpus Callosum - immunology</topic><topic>Corpus Callosum - metabolism</topic><topic>Corpus Callosum - physiopathology</topic><topic>cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - drug effects</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Encephalitis - immunology</topic><topic>Encephalitis - metabolism</topic><topic>Encephalitis - physiopathology</topic><topic>Female</topic><topic>Frontal Lobe - immunology</topic><topic>Frontal Lobe - metabolism</topic><topic>Frontal Lobe - physiopathology</topic><topic>glia</topic><topic>Humans</topic><topic>inflammation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microglia - drug effects</topic><topic>Microglia - immunology</topic><topic>Microglia - metabolism</topic><topic>Neurology</topic><topic>Nitrites - metabolism</topic><topic>Peptide Fragments - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lue, Lih-Fen</creatorcontrib><creatorcontrib>Rydel, Russell</creatorcontrib><creatorcontrib>Brigham, Elizabeth F.</creatorcontrib><creatorcontrib>Yang, Li-Bang</creatorcontrib><creatorcontrib>Hampel, Harald</creatorcontrib><creatorcontrib>Murphy Jr, Greer M.</creatorcontrib><creatorcontrib>Brachova, Libuse</creatorcontrib><creatorcontrib>Yan, Shi-Du</creatorcontrib><creatorcontrib>Walker, Douglas G.</creatorcontrib><creatorcontrib>Shen, Yong</creatorcontrib><creatorcontrib>Rogers, Joseph</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Glia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lue, Lih-Fen</au><au>Rydel, Russell</au><au>Brigham, Elizabeth F.</au><au>Yang, Li-Bang</au><au>Hampel, Harald</au><au>Murphy Jr, Greer M.</au><au>Brachova, Libuse</au><au>Yan, Shi-Du</au><au>Walker, Douglas G.</au><au>Shen, Yong</au><au>Rogers, Joseph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro</atitle><jtitle>Glia</jtitle><addtitle>Glia</addtitle><date>2001-07</date><risdate>2001</risdate><volume>35</volume><issue>1</issue><spage>72</spage><epage>79</epage><pages>72-79</pages><issn>0894-1491</issn><eissn>1098-1136</eissn><coden>GLIAEJ</coden><abstract>We have previously developed and characterized isolated microglia and astrocyte cultures from rapid (<4 h) brain autopsies of Alzheimer's disease (AD) and nondemented elderly control (ND) patients. In the present study, we evaluate the inflammatory repertoire of AD and ND microglia cultured from white matter (corpus callosum) and gray matter (superior frontal gyrus) with respect to three major proinflammatory cytokines, three chemokines, a classical pathway complement component, a scavenger cell growth factor, and a reactive nitrogen intermediate. Significant, dose‐dependent increases in the production of pro‐interleukin‐1β (pro‐IL‐1β), interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), monocyte chemoattractant protein‐1 (MCP‐1), macrophage inflammatory peptide‐1α (MIP‐1α), IL‐8, and macrophage colony‐stimulating factor (M‐CSF) were observed after exposure to pre‐aggregated amyloid β peptide (1–42) (Aβ1–42). Across constitutive and Aβ‐stimulated conditions, secretion of complement component C1q, a reactive nitrogen intermediate, and M‐CSF was significantly higher in AD compared with ND microglia. Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators. GLIA 35:72–79, 2001. © 2001 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>11424194</pmid><doi>10.1002/glia.1072</doi><tpages>8</tpages></addata></record> |
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| subjects | Aged Aged, 80 and over Aging - immunology Aging - metabolism Aging - pathology Alzheimer Disease - immunology Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Amyloid beta-Peptides - pharmacology Biological and medical sciences Biomarkers - analysis Brain - immunology Brain - metabolism Brain - physiopathology cell culture Cells, Cultured - drug effects Cells, Cultured - immunology Cells, Cultured - metabolism chemokines Chemokines - biosynthesis complement Complement C1q - biosynthesis Complement C1q - drug effects Corpus Callosum - immunology Corpus Callosum - metabolism Corpus Callosum - physiopathology cytokines Cytokines - biosynthesis Cytokines - drug effects Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Encephalitis - immunology Encephalitis - metabolism Encephalitis - physiopathology Female Frontal Lobe - immunology Frontal Lobe - metabolism Frontal Lobe - physiopathology glia Humans inflammation Male Medical sciences Microglia - drug effects Microglia - immunology Microglia - metabolism Neurology Nitrites - metabolism Peptide Fragments - pharmacology |
| title | Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro |
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