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 : 000311 ( PubMed/Corpus ); précédent : 000310; suivant : 000312Epigallocatechin-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 ; Bao-Jian Liu ; Cun-Lian Wang ; Guo-Hua Wang ; Yong Tian ; Shao-Hua Wang ; Jun Li ; Pei-Yao Li ; Rui-Hua Zhang ; Dong Wei ; Shu-Fei Tian ; Tong XuSource :
- International immunopharmacology [ 1878-1705 ] ; 2017.
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
Links to Exploration step
pubmed:28858723Le document en format XML
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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>
</front>
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<ISOAbbreviation>Int. Immunopharmacol.</ISOAbbreviation>
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<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>
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<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>
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<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>
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<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>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<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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