Epigallocatechin-3-gallate inhibits TLR4 signaling through the 67-kDa laminin receptor and effectively alleviates acute lung injury induced by H9N2 swine influenza virus.
Identifieur interne : 000B01 ( Main/Exploration ); précédent : 000B00; suivant : 000B02Epigallocatechin-3-gallate inhibits TLR4 signaling through the 67-kDa laminin receptor and effectively alleviates acute lung injury induced by H9N2 swine influenza virus.
Auteurs : Ming-Ju Xu [République populaire de Chine] ; Bao-Jian Liu [République populaire de Chine] ; Cun-Lian Wang [République populaire de Chine] ; Guo-Hua Wang [République populaire de Chine] ; Yong Tian [République populaire de Chine] ; Shao-Hua Wang [République populaire de Chine] ; Jun Li [République populaire de Chine] ; Pei-Yao Li [République populaire de Chine] ; Rui-Hua Zhang [République populaire de Chine] ; Dong Wei [République populaire de Chine] ; Shu-Fei Tian [République populaire de Chine] ; Tong Xu [République populaire de Chine]Source :
- International immunopharmacology [ 1878-1705 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (usage thérapeutique), Catéchine (analogues et dérivés), Catéchine (usage thérapeutique), Facteur de transcription NF-kappa B (métabolisme), Femelle, Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (traitement médicamenteux), Lésion pulmonaire aigüe (immunologie), Lésion pulmonaire aigüe (traitement médicamenteux), Médiateurs de l'inflammation (métabolisme), Poumon (), Récepteur de type Toll-4 (métabolisme), Récepteur laminine (métabolisme), Régulation de l'expression des gènes, Souris, Souris de lignée BALB C, Sous-type H9N2 du virus de la grippe A (physiologie), Stress oxydatif, Suidae, Transduction du signal.
- MESH :
- analogues et dérivés : Catéchine.
- immunologie : Infections à Orthomyxoviridae, Lésion pulmonaire aigüe.
- métabolisme : Facteur de transcription NF-kappa B, Médiateurs de l'inflammation, Récepteur de type Toll-4, Récepteur laminine.
- physiologie : Sous-type H9N2 du virus de la grippe A.
- traitement médicamenteux : Infections à Orthomyxoviridae, Lésion pulmonaire aigüe.
- usage thérapeutique : Antiviraux, Catéchine.
- Animaux, Femelle, Poumon, Régulation de l'expression des gènes, Souris, Souris de lignée BALB C, Stress oxydatif, Suidae, Transduction du signal.
English descriptors
- KwdEn :
- Acute Lung Injury (drug therapy), Acute Lung Injury (immunology), Animals, Antiviral Agents (therapeutic use), Catechin (analogs & derivatives), Catechin (therapeutic use), Female, Gene Expression Regulation, Inflammation Mediators (metabolism), Influenza A Virus, H9N2 Subtype (physiology), Lung (drug effects), Mice, Mice, Inbred BALB C, NF-kappa B (metabolism), Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (immunology), Oxidative Stress, Receptors, Laminin (metabolism), Signal Transduction, Swine, Toll-Like Receptor 4 (metabolism).
- MESH :
- chemical , analogs & derivatives : Catechin.
- chemical , metabolism : Inflammation Mediators, NF-kappa B, Receptors, Laminin, Toll-Like Receptor 4.
- chemical , therapeutic use : Antiviral Agents, Catechin.
- drug effects : Lung.
- drug therapy : Acute Lung Injury, Orthomyxoviridae Infections.
- immunology : Acute Lung Injury, Orthomyxoviridae Infections.
- physiology : Influenza A Virus, H9N2 Subtype.
- Animals, Female, Gene Expression Regulation, Mice, Mice, Inbred BALB C, Oxidative Stress, Signal Transduction, Swine.
Abstract
Epigallocatechin-3-gallate (EGCG) was found to inhibit the Toll-like receptor 4 (TLR4) pathway involved in influenza virus pathogenesis. Here, the effect of EGCG on TLR4 in an H9N2 virus-induced acute lung injury mouse model was investigated. BALB/c mice were inoculated intranasally with A/Swine/Hebei/108/2002 (H9N2) virus or noninfectious allantoic fluid, and treated with EGCG and E5564 or normal saline orally for 5 consecutive days. PMVECs were treated with EGCG or anti-67kDa laminin receptor (LR). Lung physiopathology, inflammation, oxidative stress, viral replication, and TLR4/NF-κB/Toll-interacting protein (Tollip) pathway in lung tissue and/or PMVECs were investigated. EGCG attenuated lung histological lesions, decreased lung W/D ratio, cytokines levels, and inhibited MPO activity and prolonged mouse survival. EGCG treatment also markedly downregulated TLR4 and NF-κB protein levels but Tollip expression was upregulated compared with that in untreated H9N2-infected mice (P<0.05). In PMVECs, anti-67LR antibody treatment significantly downregulated Tollip levels; however, the TLR4 and NF-κB protein levels dramatically increased compared with that in the EGCG-treated group (P<0.05). EGCG remarkably downregulated TLR4 protein levels through 67LR/Tollip, decreased MPO activity and inflammatory cytokine levels, supporting EGCG as a potential therapeutic agent for managing acute lung injury induced by H9N2 SIV.
DOI: 10.1016/j.intimp.2017.08.023
PubMed: 28858723
Affiliations:
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Le document en format XML
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075131</wicri:regionArea><wicri:noRegion>Zhangjiakou 075131</wicri:noRegion></affiliation></author><author><name sortKey="Wei, Dong" sort="Wei, Dong" uniqKey="Wei D" first="Dong" last="Wei">Dong Wei</name><affiliation wicri:level="1"><nlm:affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Animal Science College, Hebei North University, Zhangjiakou 075131</wicri:regionArea><wicri:noRegion>Zhangjiakou 075131</wicri:noRegion></affiliation></author><author><name sortKey="Tian, Shu Fei" sort="Tian, Shu Fei" uniqKey="Tian S" first="Shu-Fei" last="Tian">Shu-Fei Tian</name><affiliation wicri:level="1"><nlm:affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Animal Science College, Hebei North University, Zhangjiakou 075131</wicri:regionArea><wicri:noRegion>Zhangjiakou 075131</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Tong" sort="Xu, Tong" uniqKey="Xu T" first="Tong" last="Xu">Tong Xu</name><affiliation wicri:level="1"><nlm:affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China. Electronic address: xutong1969@sohu.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Animal Science College, Hebei North University, Zhangjiakou 075131</wicri:regionArea><wicri:noRegion>Zhangjiakou 075131</wicri:noRegion></affiliation></author></analytic><series><title level="j">International immunopharmacology</title><idno type="eISSN">1878-1705</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (drug therapy)</term><term>Acute Lung Injury (immunology)</term><term>Animals</term><term>Antiviral Agents (therapeutic use)</term><term>Catechin (analogs & derivatives)</term><term>Catechin (therapeutic use)</term><term>Female</term><term>Gene Expression Regulation</term><term>Inflammation Mediators (metabolism)</term><term>Influenza A Virus, H9N2 Subtype (physiology)</term><term>Lung (drug effects)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>NF-kappa B (metabolism)</term><term>Orthomyxoviridae Infections (drug therapy)</term><term>Orthomyxoviridae Infections (immunology)</term><term>Oxidative Stress</term><term>Receptors, Laminin (metabolism)</term><term>Signal Transduction</term><term>Swine</term><term>Toll-Like Receptor 4 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antiviraux (usage thérapeutique)</term><term>Catéchine (analogues et dérivés)</term><term>Catéchine (usage thérapeutique)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Femelle</term><term>Infections à Orthomyxoviridae (immunologie)</term><term>Infections à Orthomyxoviridae (traitement médicamenteux)</term><term>Lésion pulmonaire aigüe (immunologie)</term><term>Lésion pulmonaire aigüe (traitement médicamenteux)</term><term>Médiateurs de l'inflammation (métabolisme)</term><term>Poumon ()</term><term>Récepteur de type Toll-4 (métabolisme)</term><term>Récepteur laminine (métabolisme)</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Sous-type H9N2 du virus de la grippe A (physiologie)</term><term>Stress oxydatif</term><term>Suidae</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Catechin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Inflammation Mediators</term><term>NF-kappa B</term><term>Receptors, Laminin</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiviral Agents</term><term>Catechin</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Catéchine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acute Lung Injury</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Acute Lung Injury</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term><term>Médiateurs de l'inflammation</term><term>Récepteur de type Toll-4</term><term>Récepteur laminine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Sous-type H9N2 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H9N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antiviraux</term><term>Catéchine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Gene Expression Regulation</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Oxidative Stress</term><term>Signal Transduction</term><term>Swine</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Poumon</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Stress oxydatif</term><term>Suidae</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Epigallocatechin-3-gallate (EGCG) was found to inhibit the Toll-like receptor 4 (TLR4) pathway involved in influenza virus pathogenesis. Here, the effect of EGCG on TLR4 in an H9N2 virus-induced acute lung injury mouse model was investigated. BALB/c mice were inoculated intranasally with A/Swine/Hebei/108/2002 (H9N2) virus or noninfectious allantoic fluid, and treated with EGCG and E5564 or normal saline orally for 5 consecutive days. PMVECs were treated with EGCG or anti-67kDa laminin receptor (LR). Lung physiopathology, inflammation, oxidative stress, viral replication, and TLR4/NF-κB/Toll-interacting protein (Tollip) pathway in lung tissue and/or PMVECs were investigated. EGCG attenuated lung histological lesions, decreased lung W/D ratio, cytokines levels, and inhibited MPO activity and prolonged mouse survival. EGCG treatment also markedly downregulated TLR4 and NF-κB protein levels but Tollip expression was upregulated compared with that in untreated H9N2-infected mice (P<0.05). In PMVECs, anti-67LR antibody treatment significantly downregulated Tollip levels; however, the TLR4 and NF-κB protein levels dramatically increased compared with that in the EGCG-treated group (P<0.05). EGCG remarkably downregulated TLR4 protein levels through 67LR/Tollip, decreased MPO activity and inflammatory cytokine levels, supporting EGCG as a potential therapeutic agent for managing acute lung injury induced by H9N2 SIV.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Xu, Ming Ju" sort="Xu, Ming Ju" uniqKey="Xu M" first="Ming-Ju" last="Xu">Ming-Ju Xu</name></noRegion><name sortKey="Li, Jun" sort="Li, Jun" uniqKey="Li J" first="Jun" last="Li">Jun Li</name><name sortKey="Li, Pei Yao" sort="Li, Pei Yao" uniqKey="Li P" first="Pei-Yao" last="Li">Pei-Yao Li</name><name sortKey="Liu, Bao Jian" sort="Liu, Bao Jian" uniqKey="Liu B" first="Bao-Jian" last="Liu">Bao-Jian Liu</name><name sortKey="Tian, Shu Fei" sort="Tian, Shu Fei" uniqKey="Tian S" first="Shu-Fei" last="Tian">Shu-Fei Tian</name><name sortKey="Tian, Yong" sort="Tian, Yong" uniqKey="Tian Y" first="Yong" last="Tian">Yong Tian</name><name sortKey="Wang, Cun Lian" sort="Wang, Cun Lian" uniqKey="Wang C" first="Cun-Lian" last="Wang">Cun-Lian Wang</name><name sortKey="Wang, Guo Hua" sort="Wang, Guo Hua" uniqKey="Wang G" first="Guo-Hua" last="Wang">Guo-Hua Wang</name><name sortKey="Wang, Shao Hua" sort="Wang, Shao Hua" uniqKey="Wang S" first="Shao-Hua" last="Wang">Shao-Hua Wang</name><name sortKey="Wei, Dong" sort="Wei, Dong" uniqKey="Wei D" first="Dong" last="Wei">Dong Wei</name><name sortKey="Xu, Tong" sort="Xu, Tong" uniqKey="Xu T" first="Tong" last="Xu">Tong Xu</name><name sortKey="Zhang, Rui Hua" sort="Zhang, Rui Hua" uniqKey="Zhang R" first="Rui-Hua" last="Zhang">Rui-Hua Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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