Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production ▿†
Identifieur interne : 004E81 ( Main/Exploration ); précédent : 004E80; suivant : 004E82Filarial Lymphatic Pathology Reflects Augmented Toll-Like Receptor-Mediated, Mitogen-Activated Protein Kinase-Mediated Proinflammatory Cytokine Production ▿†
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 ] ; 2011.
Descripteurs français
- KwdFr :
- Adulte, Adulte d'âge moyen, Cytokines (génétique), Cytokines (métabolisme), Femelle, Filariose lymphatique (anatomopathologie), Filariose lymphatique (immunologie), Humains, Inflammation (métabolisme), Jeune adulte, Mitogen-Activated Protein Kinase Kinases (génétique), Mitogen-Activated Protein Kinase Kinases (métabolisme), Mâle, Récepteurs de type Toll (métabolisme), Régulation de l'expression des gènes (immunologie), Sujet âgé, Système lymphatique (anatomopathologie), Système lymphatique (immunologie), Système lymphatique (parasitologie).
- MESH :
- anatomopathologie : Filariose lymphatique, Système lymphatique.
- génétique : Cytokines, Mitogen-Activated Protein Kinase Kinases.
- immunologie : Filariose lymphatique, Régulation de l'expression des gènes, Système lymphatique.
- métabolisme : Cytokines, Inflammation, Mitogen-Activated Protein Kinase Kinases, Récepteurs de type Toll.
- parasitologie : Système lymphatique.
- Adulte, Adulte d'âge moyen, Femelle, Humains, Jeune adulte, Mâle, Sujet âgé.
English descriptors
- KwdEn :
- Adult, Aged, Cytokines (genetics), Cytokines (metabolism), Elephantiasis, Filarial (immunology), Elephantiasis, Filarial (pathology), Female, Gene Expression Regulation (immunology), Humans, Inflammation (metabolism), Lymphatic System (immunology), Lymphatic System (parasitology), Lymphatic System (pathology), Male, Middle Aged, Mitogen-Activated Protein Kinase Kinases (genetics), Mitogen-Activated Protein Kinase Kinases (metabolism), Toll-Like Receptors (metabolism), Young Adult.
- MESH :
- chemical , genetics : Cytokines, Mitogen-Activated Protein Kinase Kinases.
- chemical , metabolism : Cytokines, Mitogen-Activated Protein Kinase Kinases, Toll-Like Receptors.
- immunology : Elephantiasis, Filarial, Gene Expression Regulation, Lymphatic System.
- metabolism : Inflammation.
- parasitology : Lymphatic System.
- pathology : Elephantiasis, Filarial, Lymphatic System.
- Adult, Aged, Female, Humans, Male, Middle Aged, Young Adult.
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
Affiliations:
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Le document en format XML
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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><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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