Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production ▿†
Identifieur interne : 002E48 ( Pmc/Corpus ); précédent : 002E47; suivant : 002E49Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production ▿†
Auteurs : Subash Babu ; R. Anuradha ; N. Pavan Kumar ; P. Jovvian George ; V. Kumaraswami ; Thomas B. NutmanSource :
- Infection and Immunity [ 0019-9567 ] ; 2011.
Abstract
Lymphatic filariasis can be associated with the development of serious pathology in the form of lymphedema, hydrocele, and elephantiasis in a subset of infected patients. Toll-like receptors (TLRs) are thought to play a major role in the development of filarial pathology. To elucidate the role of TLRs in the development of lymphatic pathology, we examined cytokine responses to different Toll ligands in patients with chronic lymphatic pathology (CP), infected patients with subclinical pathology (INF), and uninfected, endemic-normal (EN) individuals. TLR2, -7, and -9 ligands induced significantly elevated production of Th1 and other proinflammatory cytokines in CP patients in comparison to both INF and EN patients. TLR adaptor expression was not significantly different among the groups; however, both TLR2 and TLR9 ligands induced significantly higher levels of phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein (MAP) kinases (MAPK) as well as increased activation of NF-κB in CP individuals. Pharmacologic inhibition of both ERK1/2 and p38 MAP kinase pathways resulted in significantly diminished production of proinflammatory cytokines in CP individuals. Our data, therefore, strongly suggest an important role for TLR2- and TLR9-mediated proinflammatory cytokine induction and activation of both the MAPK and NF-κB pathways in the development of pathology in human lymphatic filariasis.
Url:
DOI: 10.1128/IAI.05419-11
PubMed: 21875961
PubMed Central: 3257941
Links to Exploration step
PMC:3257941Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production
<xref ref-type="fn" rid="FN2"><sup>▿</sup>
</xref>
<xref ref-type="fn" rid="FN1">†</xref>
</title>
<author><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name>
<affiliation><nlm:aff id="aff1">International Center for Excellence in Research, National Institutes of Health, Chennai, India</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff3">SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland</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">International Center for Excellence in Research, National Institutes of Health, 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">International Center for Excellence in Research, National Institutes of Health, 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">International Center for Excellence in Research, National Institutes of Health, 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="aff4">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 Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">21875961</idno>
<idno type="pmc">3257941</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257941</idno>
<idno type="RBID">PMC:3257941</idno>
<idno type="doi">10.1128/IAI.05419-11</idno>
<date when="2011">2011</date>
<idno type="wicri:Area/Pmc/Corpus">002E48</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002E48</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production
<xref ref-type="fn" rid="FN2"><sup>▿</sup>
</xref>
<xref ref-type="fn" rid="FN1">†</xref>
</title>
<author><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name>
<affiliation><nlm:aff id="aff1">International Center for Excellence in Research, National Institutes of Health, Chennai, India</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff3">SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland</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">International Center for Excellence in Research, National Institutes of Health, 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">International Center for Excellence in Research, National Institutes of Health, 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">International Center for Excellence in Research, National Institutes of Health, 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="aff4">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 Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</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="2011">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Lymphatic filariasis can be associated with the development of serious pathology in the form of lymphedema, hydrocele, and elephantiasis in a subset of infected patients. Toll-like receptors (TLRs) are thought to play a major role in the development of filarial pathology. To elucidate the role of TLRs in the development of lymphatic pathology, we examined cytokine responses to different Toll ligands in patients with chronic lymphatic pathology (CP), infected patients with subclinical pathology (INF), and uninfected, endemic-normal (EN) individuals. TLR2, -7, and -9 ligands induced significantly elevated production of Th1 and other proinflammatory cytokines in CP patients in comparison to both INF and EN patients. TLR adaptor expression was not significantly different among the groups; however, both TLR2 and TLR9 ligands induced significantly higher levels of phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein (MAP) kinases (MAPK) as well as increased activation of NF-κB in CP individuals. Pharmacologic inhibition of both ERK1/2 and p38 MAP kinase pathways resulted in significantly diminished production of proinflammatory cytokines in CP individuals. Our data, therefore, strongly suggest an important role for TLR2- and TLR9-mediated proinflammatory cytokine induction and activation of both the MAPK and NF-κB pathways 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="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">21875961</article-id>
<article-id pub-id-type="pmc">3257941</article-id>
<article-id pub-id-type="publisher-id">5419-11</article-id>
<article-id pub-id-type="doi">10.1128/IAI.05419-11</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Fungal and Parasitic Infections</subject>
</subj-group>
</article-categories>
<title-group><article-title>Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production
<xref ref-type="fn" rid="FN2"><sup>▿</sup>
</xref>
<xref ref-type="fn" rid="FN1">†</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Babu</surname>
<given-names>Subash</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Anuradha</surname>
<given-names>R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</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>1</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>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kumaraswami</surname>
<given-names>V.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</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>2</sup>
</xref>
</contrib>
<aff id="aff1"><label>1</label>
International Center for Excellence in Research, National Institutes of Health, Chennai, India</aff>
<aff id="aff2"><label>2</label>
Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</aff>
<aff id="aff3"><label>3</label>
SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland</aff>
<aff id="aff4"><label>4</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 id="cor1"><label>*</label>
Corresponding author. Mailing address: <addr-line>NIH-ICER, Chetpet, Chennai, India</addr-line>
. Phone: <phone>91 44 28369711</phone>
. Fax: <fax>91 44 28369757</fax>
. E-mail: <email>sbabu@mail.nih.gov</email>
.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>11</month>
<year>2011</year>
</pub-date>
<volume>79</volume>
<issue>11</issue>
<fpage>4600</fpage>
<lpage>4608</lpage>
<history><date date-type="received"><day>20</day>
<month>5</month>
<year>2011</year>
</date>
<date date-type="rev-request"><day>30</day>
<month>6</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>17</day>
<month>8</month>
<year>2011</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2011, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2011</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zii01111004600.pdf"></self-uri>
<abstract><p>Lymphatic filariasis can be associated with the development of serious pathology in the form of lymphedema, hydrocele, and elephantiasis in a subset of infected patients. Toll-like receptors (TLRs) are thought to play a major role in the development of filarial pathology. To elucidate the role of TLRs in the development of lymphatic pathology, we examined cytokine responses to different Toll ligands in patients with chronic lymphatic pathology (CP), infected patients with subclinical pathology (INF), and uninfected, endemic-normal (EN) individuals. TLR2, -7, and -9 ligands induced significantly elevated production of Th1 and other proinflammatory cytokines in CP patients in comparison to both INF and EN patients. TLR adaptor expression was not significantly different among the groups; however, both TLR2 and TLR9 ligands induced significantly higher levels of phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein (MAP) kinases (MAPK) as well as increased activation of NF-κB in CP individuals. Pharmacologic inhibition of both ERK1/2 and p38 MAP kinase pathways resulted in significantly diminished production of proinflammatory cytokines in CP individuals. Our data, therefore, strongly suggest an important role for TLR2- and TLR9-mediated proinflammatory cytokine induction and activation of both the MAPK and NF-κB pathways in the development of pathology in human lymphatic filariasis.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002E48 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 002E48 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= LymphedemaV1 |flux= Pmc |étape= Corpus |type= RBID |clé= PMC:3257941 |texte= Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production ▿† }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/RBID.i -Sk "pubmed:21875961" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a LymphedemaV1
This area was generated with Dilib version V0.6.31. |