Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease
Identifieur interne : 000018 ( Pmc/Curation ); précédent : 000017; suivant : 000019Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease
Auteurs : Carmen Noelker [France, Allemagne] ; Lydie Morel [France] ; Thomas Lescot [France] ; Anke Osterloh [Allemagne] ; Daniel Alvarez-Fischer [France, Allemagne] ; Minka Breloer [Allemagne] ; Carmen Henze [France] ; Candan Depboylu [Allemagne] ; Delphine Skrzydelski [France] ; Patrick P. Michel [France] ; Richard C. Dodel [Allemagne] ; Lixia Lu [France] ; Etienne C. Hirsch [France] ; Stéphane Hunot [France] ; Andreas Hartmann [France]Source :
- Scientific Reports [ 2045-2322 ] ; 2013.
Abstract
In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.
Url:
DOI: 10.1038/srep01393
PubMed: 23462811
PubMed Central: 3589722
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Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P." last="Michel">Patrick P. 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strict</wicri:regionArea></affiliation></author><author><name sortKey="Morel, Lydie" sort="Morel, Lydie" uniqKey="Morel L" first="Lydie" last="Morel">Lydie Morel</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Lescot, Thomas" sort="Lescot, Thomas" uniqKey="Lescot T" first="Thomas" last="Lescot">Thomas Lescot</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Osterloh, Anke" sort="Osterloh, Anke" uniqKey="Osterloh A" first="Anke" last="Osterloh">Anke Osterloh</name><affiliation wicri:level="1"><nlm:aff id="a3"><institution>Bernhard Nocht Institute for Tropical Medicine</institution>, Hamburg, 20324 Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>, Hamburg</wicri:regionArea></affiliation></author><author><name sortKey="Alvarez Fischer, Daniel" sort="Alvarez Fischer, Daniel" uniqKey="Alvarez Fischer D" first="Daniel" last="Alvarez-Fischer">Daniel Alvarez-Fischer</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="a2"><institution>Department of Neurology</institution>, Philipps-University Marburg, 35043 Marburg,<country>Germany</country></nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Breloer, Minka" sort="Breloer, Minka" uniqKey="Breloer M" first="Minka" last="Breloer">Minka Breloer</name><affiliation wicri:level="1"><nlm:aff id="a3"><institution>Bernhard Nocht Institute for Tropical Medicine</institution>, Hamburg, 20324 Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>, Hamburg</wicri:regionArea></affiliation></author><author><name sortKey="Henze, Carmen" sort="Henze, Carmen" uniqKey="Henze C" first="Carmen" last="Henze">Carmen Henze</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Depboylu, Candan" sort="Depboylu, Candan" uniqKey="Depboylu C" first="Candan" last="Depboylu">Candan Depboylu</name><affiliation wicri:level="1"><nlm:aff id="a2"><institution>Department of Neurology</institution>, Philipps-University Marburg, 35043 Marburg,<country>Germany</country></nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Skrzydelski, Delphine" sort="Skrzydelski, Delphine" uniqKey="Skrzydelski D" first="Delphine" last="Skrzydelski">Delphine Skrzydelski</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P." last="Michel">Patrick P. Michel</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Dodel, Richard C" sort="Dodel, Richard C" uniqKey="Dodel R" first="Richard C." last="Dodel">Richard C. Dodel</name><affiliation wicri:level="1"><nlm:aff id="a2"><institution>Department of Neurology</institution>, Philipps-University Marburg, 35043 Marburg,<country>Germany</country></nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Lu, Lixia" sort="Lu, Lixia" uniqKey="Lu L" first="Lixia" last="Lu">Lixia Lu</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name><affiliation wicri:level="1"><nlm:aff id="a1"><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></nlm:aff><country xml:lang="fr">France</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Scientific Reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Hirsch, E C" uniqKey="Hirsch E">E. C. Hirsch</name></author><author><name sortKey="Hunot, S" uniqKey="Hunot S">S. Hunot</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcgeer, P L" uniqKey="Mcgeer P">P. L. McGeer</name></author><author><name sortKey="Itagaki, S" uniqKey="Itagaki S">S. Itagaki</name></author><author><name sortKey="Boyes, B E" uniqKey="Boyes B">B. E. Boyes</name></author><author><name sortKey="Mcgeer, E G" uniqKey="Mcgeer E">E. G. McGeer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moresco, E M" uniqKey="Moresco E">E. M. Moresco</name></author><author><name sortKey="Lavine, D" uniqKey="Lavine D">D. LaVine</name></author><author><name sortKey="Beutler, B" uniqKey="Beutler B">B. Beutler</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Laflamme, N" uniqKey="Laflamme N">N. Laflamme</name></author><author><name sortKey="Rivest, S" uniqKey="Rivest S">S. Rivest</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ros Bernal, F" uniqKey="Ros Bernal F">F. Ros-Bernal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stefanova, N" uniqKey="Stefanova N">N. Stefanova</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Beraud, D" uniqKey="Beraud D">D. Beraud</name></author><author><name sortKey="Maguire Zeiss, K A" uniqKey="Maguire Zeiss K">K. A. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Sci Rep</journal-id><journal-id journal-id-type="iso-abbrev">Sci Rep</journal-id><journal-title-group><journal-title>Scientific Reports</journal-title></journal-title-group><issn pub-type="epub">2045-2322</issn><publisher><publisher-name>Nature Publishing Group</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23462811</article-id><article-id pub-id-type="pmc">3589722</article-id><article-id pub-id-type="pii">srep01393</article-id><article-id pub-id-type="doi">10.1038/srep01393</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Noelker</surname><given-names>Carmen</given-names></name><xref ref-type="aff" rid="a1">1</xref><xref ref-type="aff" rid="a2">2</xref></contrib><contrib contrib-type="author"><name><surname>Morel</surname><given-names>Lydie</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Lescot</surname><given-names>Thomas</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Osterloh</surname><given-names>Anke</given-names></name><xref ref-type="aff" rid="a3">3</xref></contrib><contrib contrib-type="author"><name><surname>Alvarez-Fischer</surname><given-names>Daniel</given-names></name><xref ref-type="aff" rid="a1">1</xref><xref ref-type="aff" rid="a2">2</xref></contrib><contrib contrib-type="author"><name><surname>Breloer</surname><given-names>Minka</given-names></name><xref ref-type="aff" rid="a3">3</xref></contrib><contrib contrib-type="author"><name><surname>Henze</surname><given-names>Carmen</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Depboylu</surname><given-names>Candan</given-names></name><xref ref-type="aff" rid="a2">2</xref></contrib><contrib contrib-type="author"><name><surname>Skrzydelski</surname><given-names>Delphine</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Michel</surname><given-names>Patrick P.</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Dodel</surname><given-names>Richard C.</given-names></name><xref ref-type="aff" rid="a2">2</xref></contrib><contrib contrib-type="author"><name><surname>Lu</surname><given-names>Lixia</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hirsch</surname><given-names>Etienne C.</given-names></name><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hunot</surname><given-names>Stéphane</given-names></name><xref ref-type="corresp" rid="c1">a</xref><xref ref-type="aff" rid="a1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hartmann</surname><given-names>Andreas</given-names></name><xref ref-type="corresp" rid="c2">b</xref><xref ref-type="aff" rid="a1">1</xref></contrib><aff id="a1"><label>1</label><institution>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière</institution>, 75013 Paris,<country>France</country></aff><aff id="a2"><label>2</label><institution>Department of Neurology</institution>, Philipps-University Marburg, 35043 Marburg,<country>Germany</country></aff><aff id="a3"><label>3</label><institution>Bernhard Nocht Institute for Tropical Medicine</institution>, Hamburg, 20324 Germany</aff></contrib-group><author-notes><corresp id="c1"><label>a</label><email>stephane.hunot@upmc.fr</email></corresp><corresp id="c2"><label>b</label><email>andreas.hartmann@psl.aphp.fr</email></corresp></author-notes><pub-date pub-type="epub"><day>06</day><month>03</month><year>2013</year></pub-date><pub-date pub-type="collection"><year>2013</year></pub-date><volume>3</volume><elocation-id>1393</elocation-id><history><date date-type="received"><day>29</day><month>05</month><year>2012</year></date><date date-type="accepted"><day>18</day><month>01</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2013, Macmillan Publishers Limited. All rights reserved</copyright-statement><copyright-year>2013</copyright-year><copyright-holder>Macmillan Publishers Limited. All rights reserved</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-nd/3.0/"><pmc-comment>author-paid</pmc-comment>
<license-p>This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-nd/3.0/">http://creativecommons.org/licenses/by-nc-nd/3.0/</ext-link></license-p></license></permissions><abstract><p>In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.</p></abstract></article-meta></front><floats-group><fig id="f1"><label>Figure 1</label><caption><p>(A): HPLC measurement of striatal dopamine (DA) and homovanillic acid (HVA) levels, as well as calculation of the HVA/DA-ratio after MPTP-intoxication of TLR4- deficient (TLR def) and WT mice in comparison to saline treated mice.Values are expressed as mean ± SEM (*p < 0.05 comparing MPTP treated group with its saline control, #p < 0.05 comparing MPTP-treated groups of WT and TLR4-deficient mice. (B): TH-positive cell number in SN after MPTP treatment. WT = WT mice, TLR deficient = TLR4 deficient mice. Values are expressed as mean ± SEM (*p < 0.05 comparing MPTP treated group with its saline control). (C): Representative photographs of the SN of each treatment group is shown. TH-staining of free-floating cryomicrotome-cut sections at day 7. TLR4-deficient = TLR4-deficient mice, WT = wild-type mice. Control = saline treated mice, MPTP = MPTP-treated mice, Scale bars = 200 μm.</p></caption><graphic xlink:href="srep01393-f1"></graphic></fig><fig id="f2"><label>Figure 2</label><caption><p>(A): Number of nigral Iba<sup>+</sup> microglia at day 2 and day7.WT = WT mice, TLR def = TLR4-deficient mice. Values are expressed as mean ± SEM (*p < 0.05 comparing MPTP-treated group with its saline control, #p < 0.05 comparing MPTP-treated groups of WT and TLR4-deficient mice). (B): MHC II+ cell number in SN after MPTP treatment at day 2. WT = WT mice, TLR def = TLR4-deficient mice. Values are expressed as mean ± SEM (*p < 0.05 comparing MPTP-treated group with its saline control, #p < 0.05 comparing MPTP-treated groups of WT and TLR4-deficient mice). (C): Representative photographs of the SN (Iba-1 staining) of each treatment group at day 2 are shown. TLR4 <italic>def</italic> = TLR4-deficient mice, WT = wild-type mice. Control = saline treated mice, MPTP = MPTP treated mice. Scale bars = 200 μm. (D): Correlation analysis of TH<sup>+</sup>- and Iba<sup>+</sup>-positive cells counts at day 7 in SNpc (r = −0.92, p < 0.001).</p></caption><graphic xlink:href="srep01393-f2"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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