AUTOTAXIN DOWNREGULATES LPS – INDUCED MICROGLIA ACTIVATION AND PRO-INFLAMMATORY CYTOKINES PRODUCTION
Identifieur interne : 000639 ( Pmc/Corpus ); précédent : 000638; suivant : 000640AUTOTAXIN DOWNREGULATES LPS – INDUCED MICROGLIA ACTIVATION AND PRO-INFLAMMATORY CYTOKINES PRODUCTION
Auteurs : Rana Awada ; Jean Sébastien Saulnier-Blache ; Sandra Grès ; Emmanuel Bourdon ; Philippe Rondeau ; Avinash Parimisetty ; Ruben Orihuela ; G. Jean Harry ; Christian Lefebvre D EllencourtSource :
- Journal of cellular biochemistry [ 0730-2312 ] ; 2014.
Abstract
Inflammation is essential in defense against infection or injury. It is tightly regulated, as over-response can be detrimental, especially in immune-privileged organs such as the central nervous system (CNS). Microglia constitutes the major source of inflammatory factors, but are also involved in the regulation of the inflammation and in the reparation. Autotaxin (ATX), a phospholipase D, converts lysophosphatidylcholine into lysophosphatidic acid (LPA) and is upregulated in several CNS injuries. LPA, a pleiotropic immunomodulatory factor, can induce multiple cellular processes including morphological changes, proliferation, death and survival.
We investigated ATX effects on microglia inflammatory response to lipopolysaccharide (LPS), mimicking gram-negative infection. Murine BV-2 microglia and stable transfected, overexpressing ATX-BV-2 (A+) microglia were treated with LPS. Tumor necrosis factor α (TNFα), interleukin (IL)-6 and IL-10 mRNA and proteins levels were examined by qRT-PCR and ELISA, respectively. Secreted LPA was quantified by a radioenzymatic assay and microglial activation markers (CD11b, CD14, B7.1 and B7.2) were determined by flow cytometry.
ATX expression and LPA production were significantly enhanced in LPS treated BV-2 cells. LPS induction of mRNA and protein level for TNFα and IL-6 were inhibited in A+ cells, while IL-10 was increased. CD11b, CD14, and B7.1 and B7.2 expressions were reduced in A+ cells.
Our results strongly suggest deactivation of microglia and an IL-10 inhibitory of ATX with LPS induced microglia activation.
Url:
DOI: 10.1002/jcb.24889
PubMed: 25053164
PubMed Central: 4275303
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PMC:4275303Le document en format XML
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Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25053164</idno><idno type="pmc">4275303</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275303</idno><idno type="RBID">PMC:4275303</idno><idno type="doi">10.1002/jcb.24889</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000639</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000639</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">AUTOTAXIN DOWNREGULATES LPS – INDUCED MICROGLIA ACTIVATION AND PRO-INFLAMMATORY CYTOKINES PRODUCTION</title><author><name sortKey="Awada, Rana" sort="Awada, Rana" uniqKey="Awada R" first="Rana" last="Awada">Rana Awada</name><affiliation><nlm:aff id="A1">Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author><author><name sortKey="Saulnier Blache, Jean Sebastien" sort="Saulnier Blache, Jean Sebastien" uniqKey="Saulnier Blache J" first="Jean Sébastien" last="Saulnier-Blache">Jean Sébastien Saulnier-Blache</name><affiliation><nlm:aff id="A2">INSERM U1048, Institut des maladies métaboliques et cardiovasculaires (I2MC). 1 avenue Jean Poulhès, BP84225, 31432 Toulouse, Cedex 4, France</nlm:aff></affiliation></author><author><name sortKey="Gres, Sandra" sort="Gres, Sandra" uniqKey="Gres S" first="Sandra" last="Grès">Sandra Grès</name><affiliation><nlm:aff id="A2">INSERM U1048, Institut des maladies métaboliques et cardiovasculaires (I2MC). 1 avenue Jean Poulhès, BP84225, 31432 Toulouse, Cedex 4, France</nlm:aff></affiliation></author><author><name sortKey="Bourdon, Emmanuel" sort="Bourdon, Emmanuel" uniqKey="Bourdon E" first="Emmanuel" last="Bourdon">Emmanuel Bourdon</name><affiliation><nlm:aff id="A1">Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author><author><name sortKey="Rondeau, Philippe" sort="Rondeau, Philippe" uniqKey="Rondeau P" first="Philippe" last="Rondeau">Philippe Rondeau</name><affiliation><nlm:aff id="A1">Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author><author><name sortKey="Parimisetty, Avinash" sort="Parimisetty, Avinash" uniqKey="Parimisetty A" first="Avinash" last="Parimisetty">Avinash Parimisetty</name><affiliation><nlm:aff id="A1">Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author><author><name sortKey="Orihuela, Ruben" sort="Orihuela, Ruben" uniqKey="Orihuela R" first="Ruben" last="Orihuela">Ruben Orihuela</name><affiliation><nlm:aff id="A3">Neurotoxicology Group, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health, Dept. of Health and Human Services, Research Triangle Park, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Harry, G Jean" sort="Harry, G Jean" uniqKey="Harry G" first="G. Jean" last="Harry">G. Jean Harry</name><affiliation><nlm:aff id="A3">Neurotoxicology Group, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health, Dept. of Health and Human Services, Research Triangle Park, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="D Ellencourt, Christian Lefebvre" sort="D Ellencourt, Christian Lefebvre" uniqKey="D Ellencourt C" first="Christian Lefebvre" last="D Ellencourt">Christian Lefebvre D Ellencourt</name><affiliation><nlm:aff id="A1">Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of cellular biochemistry</title><idno type="ISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Inflammation is essential in defense against infection or injury. It is tightly regulated, as over-response can be detrimental, especially in immune-privileged organs such as the central nervous system (CNS). Microglia constitutes the major source of inflammatory factors, but are also involved in the regulation of the inflammation and in the reparation. Autotaxin (ATX), a phospholipase D, converts lysophosphatidylcholine into lysophosphatidic acid (LPA) and is upregulated in several CNS injuries. LPA, a pleiotropic immunomodulatory factor, can induce multiple cellular processes including morphological changes, proliferation, death and survival.</p><p id="P2">We investigated ATX effects on microglia inflammatory response to lipopolysaccharide (LPS), mimicking gram-negative infection. Murine BV-2 microglia and stable transfected, overexpressing ATX-BV-2 (A+) microglia were treated with LPS. Tumor necrosis factor α (TNFα), interleukin (IL)-6 and IL-10 mRNA and proteins levels were examined by qRT-PCR and ELISA, respectively. Secreted LPA was quantified by a radioenzymatic assay and microglial activation markers (CD11b, CD14, B7.1 and B7.2) were determined by flow cytometry.</p><p id="P3">ATX expression and LPA production were significantly enhanced in LPS treated BV-2 cells. LPS induction of mRNA and protein level for TNFα and IL-6 were inhibited in A+ cells, while IL-10 was increased. CD11b, CD14, and B7.1 and B7.2 expressions were reduced in A+ cells.</p><p id="P4">Our results strongly suggest deactivation of microglia and an IL-10 inhibitory of ATX with LPS induced microglia activation.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8205768</journal-id><journal-id journal-id-type="pubmed-jr-id">4590</journal-id><journal-id journal-id-type="nlm-ta">J Cell Biochem</journal-id><journal-id journal-id-type="iso-abbrev">J. Cell. Biochem.</journal-id><journal-title-group><journal-title>Journal of cellular biochemistry</journal-title></journal-title-group><issn pub-type="ppub">0730-2312</issn><issn pub-type="epub">1097-4644</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25053164</article-id><article-id pub-id-type="pmc">4275303</article-id><article-id pub-id-type="doi">10.1002/jcb.24889</article-id><article-id pub-id-type="manuscript">NIHMS619051</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>AUTOTAXIN DOWNREGULATES LPS – INDUCED MICROGLIA ACTIVATION AND PRO-INFLAMMATORY CYTOKINES PRODUCTION</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Awada</surname><given-names>Rana</given-names></name><email>rawada@univ-reunion.fr</email><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Saulnier-Blache</surname><given-names>Jean Sébastien</given-names></name><email>jean-sebastien.saulnier-blache@inserm.fr</email><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Grès</surname><given-names>Sandra</given-names></name><email>sandra.gres@inserm.fr</email><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Bourdon</surname><given-names>Emmanuel</given-names></name><email>Emmanuel.bourdon@univ-reunion.fr</email><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Rondeau</surname><given-names>Philippe</given-names></name><email>Philippe.rondeau@univ-reunion.fr</email><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Parimisetty</surname><given-names>Avinash</given-names></name><email>Avinash.parimisetty@univ-reunion.fr</email><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Orihuela</surname><given-names>Ruben</given-names></name><email>orihuelarg@nih.gov</email><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Harry</surname><given-names>G. Jean</given-names></name><email>harry@niehs.nih.gov</email><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>d’Hellencourt</surname><given-names>Christian Lefebvre</given-names></name><email>Christian.Lefebvre-d-Hellencourt@univ-reunion.fr</email><xref ref-type="aff" rid="A1">1</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="A1"><label>1</label>Groupe d’Etude sur l’Inflammation Chronique et l’Obésité (GEICO) EA 4516, Université de La Réunion, 15 avenue R. Cassin, CS 92003, 97715, Saint Denis Cedex and Plateforme CYROI, 2 Rue Maxime Rivière, BP 80 005, 97491 Sainte Clotilde Cedex, Reunion Island, France</aff><aff id="A2"><label>2</label>INSERM U1048, Institut des maladies métaboliques et cardiovasculaires (I2MC). 1 avenue Jean Poulhès, BP84225, 31432 Toulouse, Cedex 4, France</aff><aff id="A3"><label>3</label>Neurotoxicology Group, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health, Dept. of Health and Human Services, Research Triangle Park, North Carolina, USA</aff><author-notes><corresp id="cor1"><label>*</label><bold>Coresponding author</bold>, GEICO – EA 4516 - Université de la Réunion - 15, avenue René Cassin – CS 92003 – Cedex 09, 97715 Saint Denis de La Réunion – France, Tel: (+262) 262 93 86 48 - Fax: (+262) 262 93 82 37, <email>Christian.Lefebvre-d-Hellencourt@univ-reunion.fr</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>1</day><month>12</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>12</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>12</month><year>2015</year></pub-date><volume>115</volume><issue>12</issue><fpage>2123</fpage><lpage>2132</lpage><pmc-comment>elocation-id from pubmed: 10.1002/jcb.24889</pmc-comment>
<abstract><p id="P1">Inflammation is essential in defense against infection or injury. It is tightly regulated, as over-response can be detrimental, especially in immune-privileged organs such as the central nervous system (CNS). Microglia constitutes the major source of inflammatory factors, but are also involved in the regulation of the inflammation and in the reparation. Autotaxin (ATX), a phospholipase D, converts lysophosphatidylcholine into lysophosphatidic acid (LPA) and is upregulated in several CNS injuries. LPA, a pleiotropic immunomodulatory factor, can induce multiple cellular processes including morphological changes, proliferation, death and survival.</p><p id="P2">We investigated ATX effects on microglia inflammatory response to lipopolysaccharide (LPS), mimicking gram-negative infection. Murine BV-2 microglia and stable transfected, overexpressing ATX-BV-2 (A+) microglia were treated with LPS. Tumor necrosis factor α (TNFα), interleukin (IL)-6 and IL-10 mRNA and proteins levels were examined by qRT-PCR and ELISA, respectively. Secreted LPA was quantified by a radioenzymatic assay and microglial activation markers (CD11b, CD14, B7.1 and B7.2) were determined by flow cytometry.</p><p id="P3">ATX expression and LPA production were significantly enhanced in LPS treated BV-2 cells. LPS induction of mRNA and protein level for TNFα and IL-6 were inhibited in A+ cells, while IL-10 was increased. CD11b, CD14, and B7.1 and B7.2 expressions were reduced in A+ cells.</p><p id="P4">Our results strongly suggest deactivation of microglia and an IL-10 inhibitory of ATX with LPS induced microglia activation.</p></abstract><kwd-group><kwd>Autotaxin</kwd><kwd>microglia</kwd><kwd>inflammation</kwd><kwd>lysophosphatidic acid</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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