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 : 003D93 ( Main/Exploration ); précédent : 003D92; suivant : 003D94Toll-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, États-Unis] ; R. Anuradha [Inde] ; N. Pavan Kumar [Inde] ; P. Jovvian George [Inde] ; V. Kumaraswami [Inde] ; Thomas B. Nutman [États-Unis]Source :
- Infection and Immunity [ 0019-9567 ] ; 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.
Url:
DOI: 10.1128/IAI.06179-11
PubMed: 22508858
PubMed Central: 3416485
Affiliations:
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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><affiliations><list><country><li>Inde</li><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="Inde"><noRegion><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name></noRegion><name sortKey="Anuradha, R" sort="Anuradha, R" uniqKey="Anuradha R" first="R." last="Anuradha">R. 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></country><country name="États-Unis"><region name="Maryland"><name sortKey="Babu, Subash" sort="Babu, Subash" uniqKey="Babu S" first="Subash" last="Babu">Subash Babu</name></region><name sortKey="Nutman, Thomas B" sort="Nutman, Thomas B" uniqKey="Nutman T" first="Thomas B." last="Nutman">Thomas B. Nutman</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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