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Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE)
Microglia are the tissue macrophages of the CNS. Microglial activation coupled with macrophage infiltration is a common feature of many classic neurodegenerative disorders. The absence of cell-type specific markers has confounded and complicated the analysis of cell-type specific contributions towar...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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TheScientificWorldJOURNAL
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626137/ https://www.ncbi.nlm.nih.gov/pubmed/17982583 http://dx.doi.org/10.1100/tsw.2007.251 |
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author | Papenfuss, Tracey L. Thrash, J. Cameron Danielson, Patricia E. Foye, Pamela E. Hllbrush, Brian S. Sutcliffe, J. Gregor Whitacre, Caroline C. Carson, Monica J. |
author_facet | Papenfuss, Tracey L. Thrash, J. Cameron Danielson, Patricia E. Foye, Pamela E. Hllbrush, Brian S. Sutcliffe, J. Gregor Whitacre, Caroline C. Carson, Monica J. |
author_sort | Papenfuss, Tracey L. |
collection | PubMed |
description | Microglia are the tissue macrophages of the CNS. Microglial activation coupled with macrophage infiltration is a common feature of many classic neurodegenerative disorders. The absence of cell-type specific markers has confounded and complicated the analysis of cell-type specific contributions toward the onset, progression, and remission of neurodegeneration. Molecular screens comparing gene expression in cultured microglia and macrophages identified Golli-myelin basic protein (MBP) as a candidate molecule enriched in peripheral macrophages. In situ hybridization analysis of LPS/IFNg and experimental autoimmune encephalomyelitis (EAE)–induced CNS inflammation revealed that only a subset of CNS macrophages express Golli-MBP. Interestingly, the location and morphology of Golli-MBP+ CNS macrophages differs between these two models of CNS inflammation. These data demonstrate the difficulties of extending in vitro observations to in vivo biology and concretely illustrate the complex heterogeneity of macrophage activation states present in region- and stage-specific phases of CNS inflammation. Taken altogether, these are consistent with the emerging picture that the phenotype of CNS macrophages is actively defined by their molecular interactions with the CNS microenvironment. |
format | Text |
id | pubmed-2626137 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | TheScientificWorldJOURNAL |
record_format | MEDLINE/PubMed |
spelling | pubmed-26261372009-01-14 Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) Papenfuss, Tracey L. Thrash, J. Cameron Danielson, Patricia E. Foye, Pamela E. Hllbrush, Brian S. Sutcliffe, J. Gregor Whitacre, Caroline C. Carson, Monica J. ScientificWorldJournal Technical Report Microglia are the tissue macrophages of the CNS. Microglial activation coupled with macrophage infiltration is a common feature of many classic neurodegenerative disorders. The absence of cell-type specific markers has confounded and complicated the analysis of cell-type specific contributions toward the onset, progression, and remission of neurodegeneration. Molecular screens comparing gene expression in cultured microglia and macrophages identified Golli-myelin basic protein (MBP) as a candidate molecule enriched in peripheral macrophages. In situ hybridization analysis of LPS/IFNg and experimental autoimmune encephalomyelitis (EAE)–induced CNS inflammation revealed that only a subset of CNS macrophages express Golli-MBP. Interestingly, the location and morphology of Golli-MBP+ CNS macrophages differs between these two models of CNS inflammation. These data demonstrate the difficulties of extending in vitro observations to in vivo biology and concretely illustrate the complex heterogeneity of macrophage activation states present in region- and stage-specific phases of CNS inflammation. Taken altogether, these are consistent with the emerging picture that the phenotype of CNS macrophages is actively defined by their molecular interactions with the CNS microenvironment. TheScientificWorldJOURNAL 2007-11-02 /pmc/articles/PMC2626137/ /pubmed/17982583 http://dx.doi.org/10.1100/tsw.2007.251 Text en Copyright © 2007 Tracey L. Papenfuss et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Technical Report Papenfuss, Tracey L. Thrash, J. Cameron Danielson, Patricia E. Foye, Pamela E. Hllbrush, Brian S. Sutcliffe, J. Gregor Whitacre, Caroline C. Carson, Monica J. Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title | Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title_full | Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title_fullStr | Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title_full_unstemmed | Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title_short | Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE) |
title_sort | induction of golli-mbp expression in cns macrophages during acute lps-induced cns inflammation and experimental autoimmune encephalomyelitis (eae) |
topic | Technical Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626137/ https://www.ncbi.nlm.nih.gov/pubmed/17982583 http://dx.doi.org/10.1100/tsw.2007.251 |
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