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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Toll-Like Receptor- and Filarial Antigen-Mediated, Mitogen-Activated Protein Kinase- and NF-κB-Dependent Regulation of Angiogenic Growth Factors in Filarial Lymphatic Pathology</title><author><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Anuradha, R" sort="Anuradha, R" uniqKey="Anuradha R" first="R." last="Anuradha">R. Anuradha</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Kumar, N Pavan" sort="Kumar, N Pavan" uniqKey="Kumar N" first="N. Pavan" last="Kumar">N. Pavan Kumar</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="George, P Jovvian" sort="George, P Jovvian" uniqKey="George P" first="P. Jovvian" last="George">P. Jovvian George</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V." last="Kumaraswami">V. Kumaraswami</name><affiliation><nlm:aff id="aff3">Tuberculosis Research Center, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B." last="Nutman">Thomas B. Nutman</name><affiliation><nlm:aff id="aff2">Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22508858</idno><idno type="pmc">3416485</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416485</idno><idno type="RBID">PMC:3416485</idno><idno type="doi">10.1128/IAI.06179-11</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">002E49</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002E49</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Toll-Like Receptor- and Filarial Antigen-Mediated, Mitogen-Activated Protein Kinase- and NF-κB-Dependent Regulation of Angiogenic Growth Factors in Filarial Lymphatic Pathology</title><author><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Anuradha, R" sort="Anuradha, R" uniqKey="Anuradha R" first="R." last="Anuradha">R. Anuradha</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Kumar, N Pavan" sort="Kumar, N Pavan" uniqKey="Kumar N" first="N. Pavan" last="Kumar">N. Pavan Kumar</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="George, P Jovvian" sort="George, P Jovvian" uniqKey="George P" first="P. Jovvian" last="George">P. Jovvian George</name><affiliation><nlm:aff id="aff1">National Institutes of Health-International Center for Excellence in Research, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V." last="Kumaraswami">V. Kumaraswami</name><affiliation><nlm:aff id="aff3">Tuberculosis Research Center, Chennai, India</nlm:aff></affiliation></author><author><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B." last="Nutman">Thomas B. Nutman</name><affiliation><nlm:aff id="aff2">Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Infection and Immunity</title><idno type="ISSN">0019-9567</idno><idno type="eISSN">1098-5522</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Filarial lymphatic pathology is of multifactorial origin, with inflammation, lymphangiogenesis, and innate immune responses all playing important roles. The role of Toll-like receptors (TLRs) in the development of filarial pathology is well characterized. Similarly, the association of pathology with elevated levels of plasma angiogenic factors has also been documented. To examine the association between TLR function and the development of lymphangiogenesis in filarial infections, we examined TLR- and filarial antigen-induced expression and production of various angiogenic growth factors. We demonstrate that TLR ligands (specifically TLR2, -3, and -5 ligands) induce significantly increased expression/production of vascular endothelial growth factor A (VEGF-A) and angiopoietin-1 (Ang-1) in the peripheral blood mononuclear cells of individuals with lymphatic pathology (CP individuals) compared to that in cells of asymptomatic infected (INF) individuals. Similarly, filarial antigens induce significantly enhanced production of VEGF-C in CP compared with INF individuals. TLR2-mediated enhancement of angiogenic growth factor production in CP individuals was shown to be dependent on mitogen-activated protein kinase (MAPK) and NF-κB signaling, as pharmacologic inhibition of either extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, or NF-κB signaling resulted in significantly diminished production of VEGF-A and Ang-1. Our data therefore strongly suggest an important association between TLR signaling and lymphangiogenesis in the development of pathology in human lymphatic filariasis.</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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id><journal-id journal-id-type="iso-abbrev">Infect. Immun</journal-id><journal-id journal-id-type="hwp">iai</journal-id><journal-id journal-id-type="pmc">iai</journal-id><journal-id journal-id-type="publisher-id">IAI</journal-id><journal-title-group><journal-title>Infection and Immunity</journal-title></journal-title-group><issn pub-type="ppub">0019-9567</issn><issn pub-type="epub">1098-5522</issn><publisher><publisher-name>American Society for Microbiology</publisher-name><publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22508858</article-id><article-id pub-id-type="pmc">3416485</article-id><article-id pub-id-type="publisher-id">06179-11</article-id><article-id pub-id-type="doi">10.1128/IAI.06179-11</article-id><article-categories><subj-group subj-group-type="heading"><subject>Fungal and Parasitic Infections</subject></subj-group></article-categories><title-group><article-title>Toll-Like Receptor- and Filarial Antigen-Mediated, Mitogen-Activated Protein Kinase- and NF-κB-Dependent Regulation of Angiogenic Growth Factors in Filarial Lymphatic Pathology</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Babu</surname><given-names>Subash</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Anuradha</surname><given-names>R.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kumar</surname><given-names>N. Pavan</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>George</surname><given-names>P. Jovvian</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kumaraswami</surname><given-names>V.</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Nutman</surname><given-names>Thomas B.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><aff id="aff1"><label>a</label>National Institutes of Health-International Center for Excellence in Research, Chennai, India</aff><aff id="aff2"><label>b</label>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</aff><aff id="aff3"><label>c</label>Tuberculosis Research Center, Chennai, India</aff></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Urban</surname><given-names>J. F.</given-names><suffix>Jr.</suffix></name><role>Editor</role></contrib></contrib-group><author-notes><corresp>Address correspondence to Subash Babu, <email>sbabu@mail.nih.gov</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>2012</year></pub-date><volume>80</volume><issue>7</issue><fpage>2509</fpage><lpage>2518</lpage><history><date date-type="received"><day>14</day><month>11</month><year>2011</year></date><date date-type="rev-request"><day>19</day><month>3</month><year>2012</year></date><date date-type="accepted"><day>3</day><month>4</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2012</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zii00712002509.pdf"></self-uri><abstract><p>Filarial lymphatic pathology is of multifactorial origin, with inflammation, lymphangiogenesis, and innate immune responses all playing important roles. The role of Toll-like receptors (TLRs) in the development of filarial pathology is well characterized. Similarly, the association of pathology with elevated levels of plasma angiogenic factors has also been documented. To examine the association between TLR function and the development of lymphangiogenesis in filarial infections, we examined TLR- and filarial antigen-induced expression and production of various angiogenic growth factors. We demonstrate that TLR ligands (specifically TLR2, -3, and -5 ligands) induce significantly increased expression/production of vascular endothelial growth factor A (VEGF-A) and angiopoietin-1 (Ang-1) in the peripheral blood mononuclear cells of individuals with lymphatic pathology (CP individuals) compared to that in cells of asymptomatic infected (INF) individuals. Similarly, filarial antigens induce significantly enhanced production of VEGF-C in CP compared with INF individuals. TLR2-mediated enhancement of angiogenic growth factor production in CP individuals was shown to be dependent on mitogen-activated protein kinase (MAPK) and NF-κB signaling, as pharmacologic inhibition of either extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, or NF-κB signaling resulted in significantly diminished production of VEGF-A and Ang-1. Our data therefore strongly suggest an important association between TLR signaling and lymphangiogenesis in the development of pathology in human lymphatic filariasis.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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