Activation of vascular endothelial growth factor receptor-3 in macrophages restrains TLR4-NF-κB signaling and protects against endotoxin shock.
Identifieur interne : 002D87 ( Main/Exploration ); précédent : 002D86; suivant : 002D88Activation of vascular endothelial growth factor receptor-3 in macrophages restrains TLR4-NF-κB signaling and protects against endotoxin shock.
Auteurs : Yanbo Zhang [République populaire de Chine] ; Yao Lu [République populaire de Chine] ; Li Ma [République populaire de Chine] ; Xudong Cao [République populaire de Chine] ; Jun Xiao [République populaire de Chine] ; Jiexia Chen [République populaire de Chine] ; Shaozhuo Jiao [République populaire de Chine] ; Yunzhen Gao [République populaire de Chine] ; Chang Liu [République populaire de Chine] ; Zhaojun Duan [République populaire de Chine] ; Dangsheng Li [République populaire de Chine] ; Yulong He [République populaire de Chine] ; Bin Wei [République populaire de Chine] ; Hongyan Wang [République populaire de Chine]Source :
- Immunity [ 1097-4180 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Bactéries anaérobies à Gram négatif (immunologie), Choc septique (immunologie), Cytokines (métabolisme), Escherichia coli (immunologie), Facteur de croissance endothéliale vasculaire de type C (immunologie), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Immunité innée (génétique), Infections à Escherichia coli (immunologie), Ingénierie des protéines, Lipopolysaccharides (immunologie), Macrophages (immunologie), Modèles animaux de maladie humaine, Médiateurs de l'inflammation (métabolisme), Phosphatidylinositol 3-kinases (métabolisme), Protéine-1 suppressive de la signalisation des cytokines, Protéines SOCS (génétique), Protéines SOCS (métabolisme), Récepteur de type Toll-4 (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Salmonella typhimurium (immunologie), Salmonelloses (immunologie), Souris, Souris de lignée C57BL, Souris transgéniques, Structure tertiaire des protéines (génétique), Transduction du signal (immunologie).
- MESH :
- génétique : Immunité innée, Protéines SOCS, Récepteur-3 au facteur croissance endothéliale vasculaire, Structure tertiaire des protéines.
- immunologie : Bactéries anaérobies à Gram négatif, Choc septique, Escherichia coli, Facteur de croissance endothéliale vasculaire de type C, Infections à Escherichia coli, Lipopolysaccharides, Macrophages, Salmonella typhimurium, Salmonelloses, Transduction du signal.
- métabolisme : Cytokines, Facteur de croissance endothéliale vasculaire de type C, Facteur de transcription NF-kappa B, Médiateurs de l'inflammation, Phosphatidylinositol 3-kinases, Protéines SOCS, Récepteur de type Toll-4, Récepteur-3 au facteur croissance endothéliale vasculaire.
- Animaux, Ingénierie des protéines, Modèles animaux de maladie humaine, Protéine-1 suppressive de la signalisation des cytokines, Souris, Souris de lignée C57BL, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Cytokines (metabolism), Disease Models, Animal, Escherichia coli (immunology), Escherichia coli Infections (immunology), Gram-Negative Anaerobic Bacteria (immunology), Immunity, Innate (genetics), Inflammation Mediators (metabolism), Lipopolysaccharides (immunology), Macrophages (immunology), Mice, Mice, Inbred C57BL, Mice, Transgenic, NF-kappa B (metabolism), Phosphatidylinositol 3-Kinases (metabolism), Protein Engineering, Protein Structure, Tertiary (genetics), Salmonella Infections (immunology), Salmonella typhimurium (immunology), Shock, Septic (immunology), Signal Transduction (immunology), Suppressor of Cytokine Signaling 1 Protein, Suppressor of Cytokine Signaling Proteins (genetics), Suppressor of Cytokine Signaling Proteins (metabolism), Toll-Like Receptor 4 (metabolism), Vascular Endothelial Growth Factor C (immunology), Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , genetics : Suppressor of Cytokine Signaling Proteins, Vascular Endothelial Growth Factor Receptor-3.
- chemical , immunology : Lipopolysaccharides, Vascular Endothelial Growth Factor C.
- chemical , metabolism : Cytokines, Inflammation Mediators, NF-kappa B, Phosphatidylinositol 3-Kinases, Suppressor of Cytokine Signaling Proteins, Toll-Like Receptor 4, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-3.
- genetics : Immunity, Innate, Protein Structure, Tertiary.
- immunology : Escherichia coli, Escherichia coli Infections, Gram-Negative Anaerobic Bacteria, Macrophages, Salmonella Infections, Salmonella typhimurium, Shock, Septic, Signal Transduction.
- Animals, Disease Models, Animal, Mice, Mice, Inbred C57BL, Mice, Transgenic, Protein Engineering, Suppressor of Cytokine Signaling 1 Protein.
Abstract
Toll-like receptors (TLRs) are critical in mediating innate immune responses against infections. However, uncontrolled TLR-triggered inflammation is associated with endotoxin shock. To better understand the homeostatic mechanisms induced by TLR4 signaling, we screened a group of key cytokines, chemokines, growth factors, and their receptors for bacteria- or LPS-induced expression. The surface vascular endothelial growth factor receptor-3 (VEGFR-3) and its ligand VEGF-C were upregulated in macrophages. VEGFR-3 ligation by VEGF-C significantly attenuated proinflammatory cytokine production. Notably, ablation of the ligand-binding domain or tyrosine kinase activity of VEGFR-3 rendered mice more sensitive to septic shock. VEGFR-3 restrained TLR4-NF-κB activation by regulating the PI3-kinase-Akt signaling pathway and SOCS1 expression. Aside from targeting lymphatic vessels, we suggest a key role of VEGFR-3 on macrophages to prevent infections that is complicated with lymphoedema. Thus, VEGFR-3-VEGF-C signaling represents a "self-control" mechanism during antibacterial innate immunity.
DOI: 10.1016/j.immuni.2014.01.013
PubMed: 24656836
Affiliations:
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Le document en format XML
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<author><name sortKey="Wei, Bin" sort="Wei, Bin" uniqKey="Wei B" first="Bin" last="Wei">Bin Wei</name>
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<author><name sortKey="Wang, Hongyan" sort="Wang, Hongyan" uniqKey="Wang H" first="Hongyan" last="Wang">Hongyan Wang</name>
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<term>Disease Models, Animal</term>
<term>Escherichia coli (immunology)</term>
<term>Escherichia coli Infections (immunology)</term>
<term>Gram-Negative Anaerobic Bacteria (immunology)</term>
<term>Immunity, Innate (genetics)</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Lipopolysaccharides (immunology)</term>
<term>Macrophages (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>NF-kappa B (metabolism)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Protein Engineering</term>
<term>Protein Structure, Tertiary (genetics)</term>
<term>Salmonella Infections (immunology)</term>
<term>Salmonella typhimurium (immunology)</term>
<term>Shock, Septic (immunology)</term>
<term>Signal Transduction (immunology)</term>
<term>Suppressor of Cytokine Signaling 1 Protein</term>
<term>Suppressor of Cytokine Signaling Proteins (genetics)</term>
<term>Suppressor of Cytokine Signaling Proteins (metabolism)</term>
<term>Toll-Like Receptor 4 (metabolism)</term>
<term>Vascular Endothelial Growth Factor C (immunology)</term>
<term>Vascular Endothelial Growth Factor C (metabolism)</term>
<term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term>
<term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Bactéries anaérobies à Gram négatif (immunologie)</term>
<term>Choc septique (immunologie)</term>
<term>Cytokines (métabolisme)</term>
<term>Escherichia coli (immunologie)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (immunologie)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Immunité innée (génétique)</term>
<term>Infections à Escherichia coli (immunologie)</term>
<term>Ingénierie des protéines</term>
<term>Lipopolysaccharides (immunologie)</term>
<term>Macrophages (immunologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Protéine-1 suppressive de la signalisation des cytokines</term>
<term>Protéines SOCS (génétique)</term>
<term>Protéines SOCS (métabolisme)</term>
<term>Récepteur de type Toll-4 (métabolisme)</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term>
<term>Salmonella typhimurium (immunologie)</term>
<term>Salmonelloses (immunologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Structure tertiaire des protéines (génétique)</term>
<term>Transduction du signal (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Suppressor of Cytokine Signaling Proteins</term>
<term>Vascular Endothelial Growth Factor Receptor-3</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Lipopolysaccharides</term>
<term>Vascular Endothelial Growth Factor C</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>Inflammation Mediators</term>
<term>NF-kappa B</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Suppressor of Cytokine Signaling Proteins</term>
<term>Toll-Like Receptor 4</term>
<term>Vascular Endothelial Growth Factor C</term>
<term>Vascular Endothelial Growth Factor Receptor-3</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Immunity, Innate</term>
<term>Protein Structure, Tertiary</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Immunité innée</term>
<term>Protéines SOCS</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire</term>
<term>Structure tertiaire des protéines</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Bactéries anaérobies à Gram négatif</term>
<term>Choc septique</term>
<term>Escherichia coli</term>
<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Infections à Escherichia coli</term>
<term>Lipopolysaccharides</term>
<term>Macrophages</term>
<term>Salmonella typhimurium</term>
<term>Salmonelloses</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Escherichia coli</term>
<term>Escherichia coli Infections</term>
<term>Gram-Negative Anaerobic Bacteria</term>
<term>Macrophages</term>
<term>Salmonella Infections</term>
<term>Salmonella typhimurium</term>
<term>Shock, Septic</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term>
<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Médiateurs de l'inflammation</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines SOCS</term>
<term>Récepteur de type Toll-4</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Protein Engineering</term>
<term>Suppressor of Cytokine Signaling 1 Protein</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Ingénierie des protéines</term>
<term>Modèles animaux de maladie humaine</term>
<term>Protéine-1 suppressive de la signalisation des cytokines</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Toll-like receptors (TLRs) are critical in mediating innate immune responses against infections. However, uncontrolled TLR-triggered inflammation is associated with endotoxin shock. To better understand the homeostatic mechanisms induced by TLR4 signaling, we screened a group of key cytokines, chemokines, growth factors, and their receptors for bacteria- or LPS-induced expression. The surface vascular endothelial growth factor receptor-3 (VEGFR-3) and its ligand VEGF-C were upregulated in macrophages. VEGFR-3 ligation by VEGF-C significantly attenuated proinflammatory cytokine production. Notably, ablation of the ligand-binding domain or tyrosine kinase activity of VEGFR-3 rendered mice more sensitive to septic shock. VEGFR-3 restrained TLR4-NF-κB activation by regulating the PI3-kinase-Akt signaling pathway and SOCS1 expression. Aside from targeting lymphatic vessels, we suggest a key role of VEGFR-3 on macrophages to prevent infections that is complicated with lymphoedema. Thus, VEGFR-3-VEGF-C signaling represents a "self-control" mechanism during antibacterial innate immunity.</div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<settlement><li>Pékin</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Yanbo" sort="Zhang, Yanbo" uniqKey="Zhang Y" first="Yanbo" last="Zhang">Yanbo Zhang</name>
</noRegion>
<name sortKey="Cao, Xudong" sort="Cao, Xudong" uniqKey="Cao X" first="Xudong" last="Cao">Xudong Cao</name>
<name sortKey="Chen, Jiexia" sort="Chen, Jiexia" uniqKey="Chen J" first="Jiexia" last="Chen">Jiexia Chen</name>
<name sortKey="Duan, Zhaojun" sort="Duan, Zhaojun" uniqKey="Duan Z" first="Zhaojun" last="Duan">Zhaojun Duan</name>
<name sortKey="Gao, Yunzhen" sort="Gao, Yunzhen" uniqKey="Gao Y" first="Yunzhen" last="Gao">Yunzhen Gao</name>
<name sortKey="He, Yulong" sort="He, Yulong" uniqKey="He Y" first="Yulong" last="He">Yulong He</name>
<name sortKey="Jiao, Shaozhuo" sort="Jiao, Shaozhuo" uniqKey="Jiao S" first="Shaozhuo" last="Jiao">Shaozhuo Jiao</name>
<name sortKey="Li, Dangsheng" sort="Li, Dangsheng" uniqKey="Li D" first="Dangsheng" last="Li">Dangsheng Li</name>
<name sortKey="Liu, Chang" sort="Liu, Chang" uniqKey="Liu C" first="Chang" last="Liu">Chang Liu</name>
<name sortKey="Lu, Yao" sort="Lu, Yao" uniqKey="Lu Y" first="Yao" last="Lu">Yao Lu</name>
<name sortKey="Ma, Li" sort="Ma, Li" uniqKey="Ma L" first="Li" last="Ma">Li Ma</name>
<name sortKey="Wang, Hongyan" sort="Wang, Hongyan" uniqKey="Wang H" first="Hongyan" last="Wang">Hongyan Wang</name>
<name sortKey="Wei, Bin" sort="Wei, Bin" uniqKey="Wei B" first="Bin" last="Wei">Bin Wei</name>
<name sortKey="Xiao, Jun" sort="Xiao, Jun" uniqKey="Xiao J" first="Jun" last="Xiao">Jun Xiao</name>
</country>
</tree>
</affiliations>
</record>
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