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 : 000310 ( PubMed/Curation ); précédent : 000309; suivant : 000311Epigallocatechin-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
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<term>Antiviraux (usage thérapeutique)</term>
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<term>Facteur de transcription NF-kappa B (métabolisme)</term>
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<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>
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</JournalIssue>
<Title>International immunopharmacology</Title>
<ISOAbbreviation>Int. Immunopharmacol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Epigallocatechin-3-gallate inhibits TLR4 signaling through the 67-kDa laminin receptor and effectively alleviates acute lung injury induced by H9N2 swine influenza virus.</ArticleTitle>
<Pagination><MedlinePgn>24-33</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S1567-5769(17)30323-5</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.intimp.2017.08.023</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Ming-Ju</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Bao-Jian</ForeName>
<Initials>BJ</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Cun-Lian</ForeName>
<Initials>CL</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Guo-Hua</ForeName>
<Initials>GH</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tian</LastName>
<ForeName>Yong</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Shao-Hua</ForeName>
<Initials>SH</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jun</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Pei-Yao</ForeName>
<Initials>PY</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Rui-Hua</ForeName>
<Initials>RH</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Dong</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tian</LastName>
<ForeName>Shu-Fei</ForeName>
<Initials>SF</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Tong</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Animal Science College, Hebei North University, Zhangjiakou 075131, PR China. Electronic address: xutong1969@sohu.com.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>08</Month>
<Day>31</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Int Immunopharmacol</MedlineTA>
<NlmUniqueID>100965259</NlmUniqueID>
<ISSNLinking>1567-5769</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017474">Receptors, Laminin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C493487">Tlr4 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>8R1V1STN48</RegistryNumber>
<NameOfSubstance UI="D002392">Catechin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>BQM438CTEL</RegistryNumber>
<NameOfSubstance UI="C045651">epigallocatechin gallate</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D055371" MajorTopicYN="N">Acute Lung Injury</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002392" MajorTopicYN="N">Catechin</DescriptorName>
<QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053127" MajorTopicYN="N">Influenza A Virus, H9N2 Subtype</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017474" MajorTopicYN="N">Receptors, Laminin</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013552" MajorTopicYN="N">Swine</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051197" MajorTopicYN="N">Toll-Like Receptor 4</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">67-kDa laminin receptor</Keyword>
<Keyword MajorTopicYN="N">Acute lung injury</Keyword>
<Keyword MajorTopicYN="N">Epigallocatechin-3-gallate</Keyword>
<Keyword MajorTopicYN="N">H9N2 swine influenza virus</Keyword>
<Keyword MajorTopicYN="N">Oxidative stress</Keyword>
<Keyword MajorTopicYN="N">Toll-like receptor 4</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>06</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2017</Year>
<Month>08</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>08</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>9</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>6</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>9</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">28858723</ArticleId>
<ArticleId IdType="pii">S1567-5769(17)30323-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.intimp.2017.08.023</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
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