FcepsilonRII/CD23 is expressed in Parkinson's disease and induces, in vitro, production of nitric oxide and tumor necrosis factor-alpha in glial cells.
Identifieur interne : 003C53 ( Main/Curation ); précédent : 003C52; suivant : 003C54FcepsilonRII/CD23 is expressed in Parkinson's disease and induces, in vitro, production of nitric oxide and tumor necrosis factor-alpha in glial cells.
Auteurs : S. Hunot [France] ; N. Dugas ; B. Faucheux ; A. Hartmann ; M. Tardieu ; P. Debré ; Yves Agid [France] ; B. Dugas ; E C HirschSource :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 0270-6474 ] ; 1999.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Female, Gene Expression Regulation (immunology), Humans, Interferon-gamma (pharmacology), Interleukin-1 (pharmacology), Levodopa (therapeutic use), Male, Middle Aged, Neuroglia (immunology), Neuroglia (metabolism), Neuroglia (pathology), Nitric Oxide (metabolism), Nitric Oxide Synthase (metabolism), Nitric Oxide Synthase Type II, Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Receptors, IgE (analysis), Receptors, IgE (metabolism), Reference Values, Reverse Transcriptase Polymerase Chain Reaction, Substantia Nigra (immunology), Substantia Nigra (metabolism), Substantia Nigra (pathology), Tumor Necrosis Factor-alpha (biosynthesis), Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (pharmacology).
- MESH :
- chemical , analysis : Receptors, IgE.
- chemical , biosynthesis : Tumor Necrosis Factor-alpha.
- chemical , genetics : Tumor Necrosis Factor-alpha.
- chemical , metabolism : Nitric Oxide, Nitric Oxide Synthase, Receptors, IgE.
- chemical , pharmacology : Interferon-gamma, Interleukin-1, Tumor Necrosis Factor-alpha.
- immunology : Gene Expression Regulation, Neuroglia, Parkinson Disease, Substantia Nigra.
- metabolism : Neuroglia, Parkinson Disease, Substantia Nigra.
- pathology : Neuroglia, Parkinson Disease, Substantia Nigra.
- chemical , therapeutic use : Levodopa.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Nitric Oxide Synthase Type II, Reference Values, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
Oxidative stress is thought to be involved in the mechanism of nerve cell death in Parkinson's disease (PD). Among several toxic oxidative species, nitric oxide (NO) has been proposed as a key element on the basis of the increased density of glial cells expressing inducible nitric oxide synthase (iNOS) in the substantia nigra (SN) of patients with PD. However, the mechanism of iNOS induction in the CNS is poorly understood, especially under pathological conditions. Because cytokines and FcepsilonRII/CD23 antigen have been implicated in the induction of iNOS in the immune system, we investigated their role in glial cells in vitro and in the SN of patients with PD and matched control subjects. We show that, in vitro, interferon-gamma (IFN-gamma) together with interleukin-1beta (Il-1beta) and tumor necrosis factor-alpha (TNF-alpha) can induce the expression of CD23 in glial cells. Ligation of CD23 with specific antibodies resulted in the induction of iNOS and the subsequent release of NO. The activation of CD23 also led to an upregulation of TNF-alpha production, which was dependent on NO release. In the SN of PD patients, a significant increase in the density of glial cells expressing TNF-alpha, Il-1beta, and IFN-gamma was observed. Furthermore, although CD23 was not detectable in the SN of control subjects, it was found in both astroglial and microglial cells in parkinsonian patients. Altogether, these data demonstrate the existence of a cytokine/CD23-dependent activation pathway of iNOS and of proinflammatory mediators in glial cells and their involvement in the pathophysiology of PD.
PubMed: 10212304
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pubmed:10212304Le document en format XML
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Hunot</name><affiliation wicri:level="3"><nlm:affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, F-75013 Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Institut National de la Santé et de la Recherche Médicale, Unité 289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, F-75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Dugas, N" sort="Dugas, N" uniqKey="Dugas N" first="N" last="Dugas">N. Dugas</name></author><author><name sortKey="Faucheux, B" sort="Faucheux, B" uniqKey="Faucheux B" first="B" last="Faucheux">B. Faucheux</name></author><author><name sortKey="Hartmann, A" sort="Hartmann, A" uniqKey="Hartmann A" first="A" last="Hartmann">A. 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Dugas</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></analytic><series><title level="j">The Journal of neuroscience : the official journal of the Society for Neuroscience</title><idno type="ISSN">0270-6474</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Gene Expression Regulation (immunology)</term><term>Humans</term><term>Interferon-gamma (pharmacology)</term><term>Interleukin-1 (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Neuroglia (immunology)</term><term>Neuroglia (metabolism)</term><term>Neuroglia (pathology)</term><term>Nitric Oxide (metabolism)</term><term>Nitric Oxide Synthase (metabolism)</term><term>Nitric Oxide Synthase Type II</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Receptors, IgE (analysis)</term><term>Receptors, IgE (metabolism)</term><term>Reference Values</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Substantia Nigra (immunology)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Tumor Necrosis Factor-alpha (biosynthesis)</term><term>Tumor Necrosis Factor-alpha (genetics)</term><term>Tumor Necrosis Factor-alpha (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Receptors, IgE</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nitric Oxide</term><term>Nitric Oxide Synthase</term><term>Receptors, IgE</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interferon-gamma</term><term>Interleukin-1</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gene Expression Regulation</term><term>Neuroglia</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neuroglia</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroglia</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nitric Oxide Synthase Type II</term><term>Reference Values</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress is thought to be involved in the mechanism of nerve cell death in Parkinson's disease (PD). Among several toxic oxidative species, nitric oxide (NO) has been proposed as a key element on the basis of the increased density of glial cells expressing inducible nitric oxide synthase (iNOS) in the substantia nigra (SN) of patients with PD. However, the mechanism of iNOS induction in the CNS is poorly understood, especially under pathological conditions. Because cytokines and FcepsilonRII/CD23 antigen have been implicated in the induction of iNOS in the immune system, we investigated their role in glial cells in vitro and in the SN of patients with PD and matched control subjects. We show that, in vitro, interferon-gamma (IFN-gamma) together with interleukin-1beta (Il-1beta) and tumor necrosis factor-alpha (TNF-alpha) can induce the expression of CD23 in glial cells. Ligation of CD23 with specific antibodies resulted in the induction of iNOS and the subsequent release of NO. The activation of CD23 also led to an upregulation of TNF-alpha production, which was dependent on NO release. In the SN of PD patients, a significant increase in the density of glial cells expressing TNF-alpha, Il-1beta, and IFN-gamma was observed. Furthermore, although CD23 was not detectable in the SN of control subjects, it was found in both astroglial and microglial cells in parkinsonian patients. Altogether, these data demonstrate the existence of a cytokine/CD23-dependent activation pathway of iNOS and of proinflammatory mediators in glial cells and their involvement in the pathophysiology of PD.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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