Toll-like receptor- and filarial antigen-mediated, mitogen-activated protein kinase- and NF-κB-dependent regulation of angiogenic growth factors in filarial lymphatic pathology.
Identifieur interne : 001D76 ( PubMed/Checkpoint ); précédent : 001D75; suivant : 001D77Toll-like receptor- and filarial antigen-mediated, mitogen-activated protein kinase- and NF-κB-dependent regulation of angiogenic growth factors in filarial lymphatic pathology.
Auteurs : Subash Babu [Inde] ; R. Anuradha ; N Pavan Kumar ; P Jovvian George ; V. Kumaraswami ; Thomas B. NutmanSource :
- Infection and immunity [ 1098-5522 ] ; 2012.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Adulte d'âge moyen, Antigènes d'helminthe (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Femelle, Filariose lymphatique (anatomopathologie), Humains, Jeune adulte, Mitogen-Activated Protein Kinases (métabolisme), Mâle, Néovascularisation pathologique, Protéines angiogéniques (métabolisme), Récepteurs de type Toll (métabolisme), Sujet âgé, Vaisseaux lymphatiques (anatomopathologie).
- MESH :
- anatomopathologie : Filariose lymphatique, Vaisseaux lymphatiques.
- métabolisme : Antigènes d'helminthe, Facteur de transcription NF-kappa B, Mitogen-Activated Protein Kinases, Protéines angiogéniques, Récepteurs de type Toll.
- Adolescent, Adulte, Adulte d'âge moyen, Femelle, Humains, Jeune adulte, Mâle, Néovascularisation pathologique, Sujet âgé.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Angiogenic Proteins (metabolism), Antigens, Helminth (metabolism), Elephantiasis, Filarial (pathology), Female, Humans, Lymphatic Vessels (pathology), Male, Middle Aged, Mitogen-Activated Protein Kinases (metabolism), NF-kappa B (metabolism), Neovascularization, Pathologic, Toll-Like Receptors (metabolism), Young Adult.
- MESH :
- chemical , metabolism : Angiogenic Proteins, Antigens, Helminth, Mitogen-Activated Protein Kinases, NF-kappa B, Toll-Like Receptors.
- pathology : Elephantiasis, Filarial, Lymphatic Vessels.
- Adolescent, Adult, Aged, Female, Humans, Male, Middle Aged, Neovascularization, Pathologic, Young Adult.
Abstract
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.
DOI: 10.1128/IAI.06179-11
PubMed: 22508858
Affiliations:
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Anuradha</name></author><author><name sortKey="Kumar, N Pavan" sort="Kumar, N Pavan" uniqKey="Kumar N" first="N Pavan" last="Kumar">N Pavan Kumar</name></author><author><name sortKey="George, P Jovvian" sort="George, P Jovvian" uniqKey="George P" first="P Jovvian" last="George">P Jovvian George</name></author><author><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V" last="Kumaraswami">V. Kumaraswami</name></author><author><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B" last="Nutman">Thomas B. Nutman</name></author></analytic><series><title level="j">Infection and immunity</title><idno type="eISSN">1098-5522</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Angiogenic Proteins (metabolism)</term><term>Antigens, Helminth (metabolism)</term><term>Elephantiasis, Filarial (pathology)</term><term>Female</term><term>Humans</term><term>Lymphatic Vessels (pathology)</term><term>Male</term><term>Middle Aged</term><term>Mitogen-Activated Protein Kinases (metabolism)</term><term>NF-kappa B (metabolism)</term><term>Neovascularization, Pathologic</term><term>Toll-Like Receptors (metabolism)</term><term>Young Adult</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Antigènes d'helminthe (métabolisme)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Femelle</term><term>Filariose lymphatique (anatomopathologie)</term><term>Humains</term><term>Jeune adulte</term><term>Mitogen-Activated Protein Kinases (métabolisme)</term><term>Mâle</term><term>Néovascularisation pathologique</term><term>Protéines angiogéniques (métabolisme)</term><term>Récepteurs de type Toll (métabolisme)</term><term>Sujet âgé</term><term>Vaisseaux lymphatiques (anatomopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Angiogenic Proteins</term><term>Antigens, Helminth</term><term>Mitogen-Activated Protein Kinases</term><term>NF-kappa B</term><term>Toll-Like Receptors</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Filariose lymphatique</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes d'helminthe</term><term>Facteur de transcription NF-kappa B</term><term>Mitogen-Activated Protein Kinases</term><term>Protéines angiogéniques</term><term>Récepteurs de type Toll</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Elephantiasis, Filarial</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neovascularization, Pathologic</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Femelle</term><term>Humains</term><term>Jeune adulte</term><term>Mâle</term><term>Néovascularisation pathologique</term><term>Sujet âgé</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22508858</PMID><DateCreated><Year>2012</Year><Month>06</Month><Day>15</Day></DateCreated><DateCompleted><Year>2012</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5522</ISSN><JournalIssue CitedMedium="Internet"><Volume>80</Volume><Issue>7</Issue><PubDate><Year>2012</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Toll-like receptor- and filarial antigen-mediated, mitogen-activated protein kinase- and NF-κB-dependent regulation of angiogenic growth factors in filarial lymphatic pathology.</ArticleTitle><Pagination><MedlinePgn>2509-18</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/IAI.06179-11</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Babu</LastName><ForeName>Subash</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>National Institutes of Health-International Center for Excellence in Research, Chennai, India. sbabu@mail.nih.gov</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anuradha</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Kumar</LastName><ForeName>N Pavan</ForeName><Initials>NP</Initials></Author><Author ValidYN="Y"><LastName>George</LastName><ForeName>P Jovvian</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Kumaraswami</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>Thomas B</ForeName><Initials>TB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042501">Angiogenic Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000947">Antigens, Helminth</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051193">Toll-Like Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Trop Med Hyg. 2010 Oct;83(4):884-90</RefSource><PMID Version="1">20889885</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 2010 Jun;43(2):59-72</RefSource><PMID Version="1">20848993</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parasite Immunol. 2001 Jul;23(7):389-99</RefSource><PMID Version="1">11472558</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2002 Mar 8;295(5561):1892-5</RefSource><PMID 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Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000947" MajorTopicYN="N">Antigens, Helminth</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020928" MajorTopicYN="N">Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051193" MajorTopicYN="N">Toll-Like Receptors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3416485</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate 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Anuradha</name><name sortKey="George, P Jovvian" sort="George, P Jovvian" uniqKey="George P" first="P Jovvian" last="George">P Jovvian George</name><name sortKey="Kumar, N Pavan" sort="Kumar, N Pavan" uniqKey="Kumar N" first="N Pavan" last="Kumar">N Pavan Kumar</name><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V" last="Kumaraswami">V. Kumaraswami</name><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B" last="Nutman">Thomas B. Nutman</name></noCountry><country name="Inde"><noRegion><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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