Regulation of astrocyte activation by glycolipids drives chronic CNS inflammation
In multiple sclerosis and experimental autoimmune encephalomyelitis, astrocytes produce lactosylceramide, a glycolipid that promotes astrocyte and microglial activation and immune cell infiltration into the CNS. Astrocytes have complex roles in health and disease, thus it is important to study the p...
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| Veröffentlicht in: | Nature medicine Jg. 20; H. 10; S. 1147 - 1156 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
New York
Nature Publishing Group US
01.10.2014
Nature Publishing Group |
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| ISSN: | 1078-8956, 1546-170X, 1546-170X |
| Online-Zugang: | Volltext |
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| Abstract | In multiple sclerosis and experimental autoimmune encephalomyelitis, astrocytes produce lactosylceramide, a glycolipid that promotes astrocyte and microglial activation and immune cell infiltration into the CNS.
Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non–cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony–stimulating factor (GM-CSF), respectively. We also detected high
B4GALT6
gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes
in vitro
. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders. |
|---|---|
| AbstractList | Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non-cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders. Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non-cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders.Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non-cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders. In multiple sclerosis and experimental autoimmune encephalomyelitis, astrocytes produce lactosylceramide, a glycolipid that promotes astrocyte and microglial activation and immune cell infiltration into the CNS. Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by β-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non–cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony–stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro . Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders. Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that lactosylceramide (LacCer) synthesized by [beta]-1,4-galactosyltransferase 6 (B4GALT6) is upregulated in the central nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). LacCer acts in an autocrine manner to control astrocyte transcriptional programs that promote neurodegeneration. In addition, LacCer in astrocytes controls the recruitment and activation of microglia and CNS-infiltrating monocytes in a non-cell autonomous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), respectively. We also detected high B4GALT6 gene expression and LacCer concentrations in CNS MS lesions. Inhibition of LacCer synthesis in mice suppressed local CNS innate immunity and neurodegeneration in EAE and interfered with the activation of human astrocytes in vitro. Thus, B4GALT6 regulates astrocyte activation and is a potential therapeutic target for MS and other neuroinflammatory disorders. |
| Audience | Academic |
| Author | Bakshi, Rohit Yeste, Ada Ellezam, Benjamin Alvarez, Jorge I Antel, Jack P Weiner, Howard L Blain, Manon Nadeau, Meghan Kivisäkk, Pia Trauger, Sunia A Quintana, Francisco J Prat, Alexandre Patel, Bonny Kallas, Keith Mayo, Lior Mascanfroni, Ivan D |
| Author_xml | – sequence: 1 givenname: Lior surname: Mayo fullname: Mayo, Lior organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 2 givenname: Sunia A surname: Trauger fullname: Trauger, Sunia A organization: FAS Center for Systems Biology, Harvard University – sequence: 3 givenname: Manon surname: Blain fullname: Blain, Manon organization: Department of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University – sequence: 4 givenname: Meghan surname: Nadeau fullname: Nadeau, Meghan organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 5 givenname: Bonny surname: Patel fullname: Patel, Bonny organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 6 givenname: Jorge I surname: Alvarez fullname: Alvarez, Jorge I organization: Department of Neuroscience, Neuroimmunology Research Lab, Center for Excellence in Neuromics, University of Montreal – sequence: 7 givenname: Ivan D surname: Mascanfroni fullname: Mascanfroni, Ivan D organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 8 givenname: Ada surname: Yeste fullname: Yeste, Ada organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 9 givenname: Pia surname: Kivisäkk fullname: Kivisäkk, Pia organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 10 givenname: Keith surname: Kallas fullname: Kallas, Keith organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 11 givenname: Benjamin surname: Ellezam fullname: Ellezam, Benjamin organization: Department of Pathology, University of Montreal and Faculty of Medicine, University of Montreal – sequence: 12 givenname: Rohit surname: Bakshi fullname: Bakshi, Rohit organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 13 givenname: Alexandre surname: Prat fullname: Prat, Alexandre organization: Department of Neuroscience, Neuroimmunology Research Lab, Center for Excellence in Neuromics, University of Montreal – sequence: 14 givenname: Jack P surname: Antel fullname: Antel, Jack P organization: Department of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University – sequence: 15 givenname: Howard L surname: Weiner fullname: Weiner, Howard L organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School – sequence: 16 givenname: Francisco J surname: Quintana fullname: Quintana, Francisco J email: fquintana@rics.bwh.harvard.edu organization: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25216636$$D View this record in MEDLINE/PubMed |
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| Snippet | In multiple sclerosis and experimental autoimmune encephalomyelitis, astrocytes produce lactosylceramide, a glycolipid that promotes astrocyte and microglial... Astrocytes have complex roles in health and disease, thus it is important to study the pathways that regulate their function. Here we report that... |
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| SubjectTerms | 13/1 13/106 13/31 13/44 14/63 631/250/262 631/250/38 64/60 82/80 96/95 Analysis Animals Antigens, CD - metabolism Astrocytes Astrocytes - immunology Astrocytes - metabolism Autoimmune diseases Biomedicine Cancer Research Cellular biology Central nervous system Central Nervous System - immunology Central Nervous System - metabolism Central Nervous System - pathology Chemokine CCL2 - genetics Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Enzymes Female Galactosyltransferases - genetics Galactosyltransferases - metabolism Gene expression Gene Knockdown Techniques Glial Fibrillary Acidic Protein Glycolipids - metabolism Humans Immunity, Innate Infectious Diseases Inflammation Inflammatory diseases Lactosylceramides - metabolism Lesions Metabolic Diseases Mice Mice, Inbred C57BL Mice, Inbred NOD Mice, Transgenic Molecular Medicine Multiple Sclerosis - genetics Multiple Sclerosis - immunology Multiple Sclerosis - metabolism Nerve Degeneration - genetics Nerve Degeneration - immunology Nerve Degeneration - metabolism Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nervous system Neurosciences Up-Regulation |
| Title | Regulation of astrocyte activation by glycolipids drives chronic CNS inflammation |
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