Alternative activation of macrophages by filarial nematodes is MyD88-independent
Identifieur interne : 005033 ( Ncbi/Merge ); précédent : 005032; suivant : 005034Alternative activation of macrophages by filarial nematodes is MyD88-independent
Auteurs : Katie J. Mylonas [Royaume-Uni] ; Marieke A. Hoeve [Royaume-Uni] ; Andrew S. Macdonald [Royaume-Uni] ; Judith E. Allen [Royaume-Uni]Source :
- Immunobiology [ 0171-2985 ] ; 2013.
Abstract
Alternative macrophage activation is largely defined by IL-4Rα stimulation but the contribution of Toll-like receptor (TLR) signaling to this phenotype is not currently known. We have investigated macrophage activation status under Th2 conditions in the absence of the core TLR adaptor molecule, MyD88. No impairment was observed in the ability of MyD88-deficient bone marrow derived macrophages to produce or express alternative activation markers, including arginase,
Url:
DOI: 10.1016/j.imbio.2012.07.006
PubMed: 22884360
PubMed Central: 3608026
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Hoeve</name><affiliation wicri:level="4"><nlm:aff id="aff0015">MRC Centre for Regenerative Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Centre for Regenerative Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author><author><name sortKey="Macdonald, Andrew S" sort="Macdonald, Andrew S" uniqKey="Macdonald A" first="Andrew S." last="Macdonald">Andrew S. Macdonald</name><affiliation wicri:level="4"><nlm:aff id="aff0005">Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author><author><name sortKey="Allen, Judith E" sort="Allen, Judith E" uniqKey="Allen J" first="Judith E." last="Allen">Judith E. Allen</name><affiliation wicri:level="4"><nlm:aff id="aff0005">Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22884360</idno><idno type="pmc">3608026</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3608026</idno><idno type="RBID">PMC:3608026</idno><idno type="doi">10.1016/j.imbio.2012.07.006</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">003F03</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003F03</idno><idno type="wicri:Area/Pmc/Curation">003F02</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">003F02</idno><idno type="wicri:Area/Pmc/Checkpoint">002513</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002513</idno><idno type="wicri:Area/Ncbi/Merge">005033</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Alternative activation of macrophages by filarial nematodes is MyD88-independent</title><author><name sortKey="Mylonas, Katie J" sort="Mylonas, Katie J" uniqKey="Mylonas K" first="Katie J." last="Mylonas">Katie J. Mylonas</name><affiliation wicri:level="1"><nlm:aff id="aff0010">The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ</wicri:regionArea><wicri:noRegion>Edinburgh EH16 4TJ</wicri:noRegion></affiliation></author><author><name sortKey="Hoeve, Marieke A" sort="Hoeve, Marieke A" uniqKey="Hoeve M" first="Marieke A." last="Hoeve">Marieke A. Hoeve</name><affiliation wicri:level="4"><nlm:aff id="aff0015">MRC Centre for Regenerative Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Centre for Regenerative Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author><author><name sortKey="Macdonald, Andrew S" sort="Macdonald, Andrew S" uniqKey="Macdonald A" first="Andrew S." last="Macdonald">Andrew S. Macdonald</name><affiliation wicri:level="4"><nlm:aff id="aff0005">Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author><author><name sortKey="Allen, Judith E" sort="Allen, Judith E" uniqKey="Allen J" first="Judith E." last="Allen">Judith E. Allen</name><affiliation wicri:level="4"><nlm:aff id="aff0005">Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT</wicri:regionArea><orgName type="university">Université d'Édimbourg</orgName><placeName><settlement type="city">Édimbourg</settlement><region type="country">Écosse</region></placeName></affiliation></author></analytic><series><title level="j">Immunobiology</title><idno type="ISSN">0171-2985</idno><idno type="eISSN">1878-3279</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>Alternative macrophage activation is largely defined by IL-4Rα stimulation but the contribution of Toll-like receptor (TLR) signaling to this phenotype is not currently known. We have investigated macrophage activation status under Th2 conditions in the absence of the core TLR adaptor molecule, MyD88. No impairment was observed in the ability of MyD88-deficient bone marrow derived macrophages to produce or express alternative activation markers, including arginase, <italic>RELM-α</italic> or <italic>Ym1</italic>, in response to IL-4 treatment <italic>in vitro</italic>. Further, we observed no difference in the ability of peritoneal exudate cells from nematode implanted wild type (WT) or MyD88-deficient mice to produce arginase or express the alternative activation markers RELM-α or Ym1. Therefore, MyD88 is not a fundamental requirement for Th2-driven macrophage alternative activation, either <italic>in vitro</italic> or <italic>in vivo</italic>.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Adachi, O" uniqKey="Adachi O">O. Adachi</name></author><author><name sortKey="Kawai, T" uniqKey="Kawai T">T. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Immunobiology</journal-id><journal-id journal-id-type="iso-abbrev">Immunobiology</journal-id><journal-title-group><journal-title>Immunobiology</journal-title></journal-title-group><issn pub-type="ppub">0171-2985</issn><issn pub-type="epub">1878-3279</issn><publisher><publisher-name>Elsevier</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22884360</article-id><article-id pub-id-type="pmc">3608026</article-id><article-id pub-id-type="publisher-id">S0171-2985(12)00170-2</article-id><article-id pub-id-type="doi">10.1016/j.imbio.2012.07.006</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Alternative activation of macrophages by filarial nematodes is MyD88-independent</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Mylonas</surname><given-names>Katie J.</given-names></name><xref rid="aff0010" ref-type="aff">b</xref><xref rid="fn0005" ref-type="fn">1</xref></contrib><contrib contrib-type="author"><name><surname>Hoeve</surname><given-names>Marieke A.</given-names></name><xref rid="aff0015" ref-type="aff">c</xref><xref rid="fn0005" ref-type="fn">1</xref></contrib><contrib contrib-type="author"><name><surname>MacDonald</surname><given-names>Andrew S.</given-names></name><xref rid="aff0005" ref-type="aff">a</xref></contrib><contrib contrib-type="author"><name><surname>Allen</surname><given-names>Judith E.</given-names></name><email>j.allen@ed.ac.uk</email><xref rid="aff0005" ref-type="aff">a</xref><xref rid="cor0005" ref-type="corresp">⁎</xref></contrib></contrib-group><aff id="aff0005"><label>a</label>Institute of Immunology and Infection Research, Centre for Immunity, Infection & Evolution, School of Biological Sciences, The University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, United Kingdom</aff><aff id="aff0010"><label>b</label>The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, United Kingdom</aff><aff id="aff0015"><label>c</label>MRC Centre for Regenerative Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, United Kingdom</aff><author-notes><corresp id="cor0005"><label>⁎</label>Corresponding author. Tel.: +44 131 650 7014. <email>j.allen@ed.ac.uk</email></corresp><fn id="fn0005"><label>1</label><p>Present address.</p></fn></author-notes><pub-date pub-type="pmc-release"><day>1</day><month>4</month><year>2013</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>4</month><year>2013</year></pub-date><volume>218</volume><issue>4</issue><fpage>570</fpage><lpage>578</lpage><history><date date-type="received"><day>13</day><month>4</month><year>2012</year></date><date date-type="rev-recd"><day>12</day><month>7</month><year>2012</year></date><date date-type="accepted"><day>14</day><month>7</month><year>2012</year></date></history><permissions><copyright-statement>© 2013 Elsevier GmbH.</copyright-statement><copyright-year>2012</copyright-year><copyright-holder>Elsevier GmbH</copyright-holder><license xlink:href="https://creativecommons.org/licenses/by/3.0/"><license-p>Open Access under <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by/3.0/">CC BY 3.0</ext-link> license</license-p></license></permissions><abstract><p>Alternative macrophage activation is largely defined by IL-4Rα stimulation but the contribution of Toll-like receptor (TLR) signaling to this phenotype is not currently known. We have investigated macrophage activation status under Th2 conditions in the absence of the core TLR adaptor molecule, MyD88. No impairment was observed in the ability of MyD88-deficient bone marrow derived macrophages to produce or express alternative activation markers, including arginase, <italic>RELM-α</italic> or <italic>Ym1</italic>, in response to IL-4 treatment <italic>in vitro</italic>. Further, we observed no difference in the ability of peritoneal exudate cells from nematode implanted wild type (WT) or MyD88-deficient mice to produce arginase or express the alternative activation markers RELM-α or Ym1. Therefore, MyD88 is not a fundamental requirement for Th2-driven macrophage alternative activation, either <italic>in vitro</italic> or <italic>in vivo</italic>.</p></abstract><kwd-group><title>Keywords</title><kwd>MyD88</kwd><kwd>TLR</kwd><kwd>Macrophage</kwd><kwd>Th2</kwd><kwd>Filariasis</kwd></kwd-group></article-meta></front><floats-group><fig id="fig0005"><label>Fig. 1</label><caption><p>MyD88 deficiency had no effect on the alternative activation of Mφ <italic>in vitro</italic>. BMMϕ were preteated o/n with IL-4 and then stimulated with LPS and IFN-γ together or separately for 16–20 h. Urea concentration is shown as a measure of arginase activity (a) and nitrite as a measure of iNOS activity (b). mRNA was extracted and realtime RT-PCR for <italic>Arginase 1</italic>, <italic>RELM-α</italic> and <italic>YM-1</italic> expression carried out. Black bars here represent IL-4 treatment (c). mRNA expression is shown as a % of a positive control sample and was normalised to β-actin. Results are shown as the mean of replicate samples (±SEM) and are representative of three experiments.</p></caption><graphic xlink:href="gr1"></graphic></fig><fig id="fig0010"><label>Fig. 2</label><caption><p>The Th1 response is impaired in MyD88<sup>−/−</sup> mice but the Th2 response is not significantly altered in <italic>B. malayi</italic>-implanted animals. Splenocytes were recovered from C57BL/6 mice 19 days after <italic>B. malayi</italic> implant or 3 days after injection with thioglycollate (thio). Splenocytes were treated with media alone, Concanavalin A (ConA) or <italic>B. malayi</italic> antigen (BMA) for 72 h before the supernatants were removed and levels of IFN-γ (a), IL-4 (b), IL-5 (c), IL-10 (d) and IL-13 (e) measured by cytometric bead array. Significant differences were determined by the Mann–Whitney test *<italic>p</italic> < 0.05, **<italic>p</italic> < 0.01. These results are representative of three experiments.</p></caption><graphic xlink:href="gr2"></graphic></fig><fig id="fig0015"><label>Fig. 3</label><caption><p>Similar numbers of Mφ, eosinophils, and lymphocytes, are found in wild type (WT) and MyD88<sup>−/−</sup> mice. 19 days after implant (3 days after thioglycollate injection; thio) PECs from mice on the C57BL/6 background were recovered and double-stained for F4/80 (a) and SiglecF (b). Sample plots are shown in (c). PECs were also stained for CD4 (d), CD8 (e) and B220 (f). Results are representative of three experiments.</p></caption><graphic xlink:href="gr3"></graphic></fig><fig id="fig0020"><label>Fig. 4</label><caption><p>No difference in the arginase activity or suppressive ability of NeMϕ in WT or MyD88<sup>−/−</sup> mice after implantation with <italic>B. malayi</italic> worms. PECs were recovered from C57BL/6 mice 19 days after <italic>B. malayi</italic> implant or 3 days after injection with thioglycollate (thio). Macrophages were purified by adherence and arginase enzyme activity calculated (a). Suppressive ability was measured by replacement of the medium and co-culture with EL-4 thymoma cells. After 48 h, the EL-4 cell proliferation was assessed by [<sup>3</sup>H] thymidine incorporation (b). Significant differences were determined by the Mann–Whitney test *<italic>p</italic> < 0.05. These results are representative of three experiments.</p></caption><graphic xlink:href="gr4"></graphic></fig><fig id="fig0025"><label>Fig. 5</label><caption><p>The absence of MyD88 had no effect on microfilaria numbers or alternative activation markers in the peritoneal cavity after <italic>B. malayi</italic> implant. At day 19 after <italic>B. malayi</italic> implant of C57BL/6 mice, i.p. lavages were carried out and numbers of microfilaria present enumerated (a). The lavage fluid was tested for RELM-α (b) and YM-1 (c) by Western blot. Macrophages were purified by adherence from peritoneal lavages and RNA extraction and realtime RT-PCR was carried out for <italic>Arginase1</italic> (d), <italic>RELM-α</italic> (e) and <italic>YM-1</italic> (f). mRNA expression is shown as a % of a positive control sample and was normalised to β-actin. These results are representative of three experiments.</p></caption><graphic xlink:href="gr5"></graphic></fig></floats-group></pmc><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Écosse</li></region><settlement><li>Édimbourg</li></settlement><orgName><li>Université d'Édimbourg</li></orgName></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Mylonas, Katie J" sort="Mylonas, Katie J" uniqKey="Mylonas K" first="Katie J." last="Mylonas">Katie J. Mylonas</name></noRegion><name sortKey="Allen, Judith E" sort="Allen, Judith E" uniqKey="Allen J" first="Judith E." last="Allen">Judith E. Allen</name><name sortKey="Hoeve, Marieke A" sort="Hoeve, Marieke A" uniqKey="Hoeve M" first="Marieke A." last="Hoeve">Marieke A. Hoeve</name><name sortKey="Macdonald, Andrew S" sort="Macdonald, Andrew S" uniqKey="Macdonald A" first="Andrew S." last="Macdonald">Andrew S. Macdonald</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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