Glutathione peroxidase-1 reduces influenza A virus-induced lung inflammation.
Identifieur interne : 000543 ( Ncbi/Merge ); précédent : 000542; suivant : 000544Glutathione peroxidase-1 reduces influenza A virus-induced lung inflammation.
Auteurs : Selcuk Yatmaz [Australie] ; Huei Jiunn Seow ; Rosa C. Gualano ; Zi Xin Wong ; John Stambas ; Stavros Selemidis ; Peter J. Crack ; Steven Bozinovski ; Gary P. Anderson ; Ross VlahosSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2013.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux, Azoles (pharmacologie), Charge virale, Chimiokines (génétique), Composés organiques du sélénium (pharmacologie), Cytokines (génétique), Espèces réactives de l'oxygène, Glutathione peroxidase (déficit), Glutathione peroxidase (génétique), Glutathione peroxidase (physiologie), Immunité acquise, Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (enzymologie), Infections à Orthomyxoviridae (étiologie), Liquide de lavage bronchoalvéolaire (cytologie), Lymphocytes T CD8+ (immunologie), Mâle, Peptide hydrolases (génétique), Pneumopathie infectieuse (), Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (enzymologie), Pneumopathie infectieuse (étiologie), Souris, Souris de lignée C57BL, Souris knockout, Sous-type H3N2 du virus de la grippe A (immunologie).
- MESH :
- anatomopathologie : Infections à Orthomyxoviridae, Pneumopathie infectieuse.
- cytologie : Liquide de lavage bronchoalvéolaire.
- déficit : Glutathione peroxidase.
- enzymologie : Infections à Orthomyxoviridae, Pneumopathie infectieuse.
- génétique : ARN messager, Chimiokines, Cytokines, Glutathione peroxidase, Peptide hydrolases.
- immunologie : Lymphocytes T CD8+, Sous-type H3N2 du virus de la grippe A.
- métabolisme : ARN messager.
- pharmacologie : Azoles, Composés organiques du sélénium.
- physiologie : Glutathione peroxidase.
- étiologie : Infections à Orthomyxoviridae, Pneumopathie infectieuse.
- Animaux, Charge virale, Espèces réactives de l'oxygène, Immunité acquise, Mâle, Pneumopathie infectieuse, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Adaptive Immunity, Animals, Azoles (pharmacology), Bronchoalveolar Lavage Fluid (cytology), CD8-Positive T-Lymphocytes (immunology), Chemokines (genetics), Cytokines (genetics), Glutathione Peroxidase (deficiency), Glutathione Peroxidase (genetics), Glutathione Peroxidase (physiology), Influenza A Virus, H3N2 Subtype (immunology), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Organoselenium Compounds (pharmacology), Orthomyxoviridae Infections (enzymology), Orthomyxoviridae Infections (etiology), Orthomyxoviridae Infections (pathology), Peptide Hydrolases (genetics), Pneumonia (enzymology), Pneumonia (etiology), Pneumonia (pathology), Pneumonia (prevention & control), RNA, Messenger (genetics), RNA, Messenger (metabolism), Reactive Oxygen Species, Viral Load.
- MESH :
- chemical , deficiency : Glutathione Peroxidase.
- chemical , genetics : Chemokines, Cytokines, Glutathione Peroxidase, Peptide Hydrolases, RNA, Messenger.
- chemical , metabolism : RNA, Messenger.
- chemical , pharmacology : Azoles, Organoselenium Compounds.
- cytology : Bronchoalveolar Lavage Fluid.
- enzymology : Orthomyxoviridae Infections, Pneumonia.
- etiology : Orthomyxoviridae Infections, Pneumonia.
- immunology : CD8-Positive T-Lymphocytes, Influenza A Virus, H3N2 Subtype.
- pathology : Orthomyxoviridae Infections, Pneumonia.
- chemical , physiology : Glutathione Peroxidase.
- prevention & control : Pneumonia.
- Adaptive Immunity, Animals, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Reactive Oxygen Species, Viral Load.
Abstract
Oxidative stress caused by excessive reactive oxygen species production is implicated in influenza A virus-induced lung disease. Glutathione peroxidase (GPx)-1 is an antioxidant enzyme that may protect lungs from such damage. The objective of this study was to determine if GPx-1 protects the lung against influenza A virus-induced lung inflammation in vivo. Male wild-type (WT) or GPx-1(-/-) mice were inoculated with HKx31 (H3N2, 1 × 10(4) plaque-forming units), and bronchoalveolar lavage fluid (BALF)/lung compartments were analyzed on Days 3 and 7 after infection for inflammatory marker expression, histology, and viral titer. WT mice infected with HKx31 had significantly more BALF total cells, macrophages, neutrophils, and lymphocytes at Days 3 and 7 compared with naive WT animals (n = 5-8; P < 0.05). However, infected GPx-1(-/-) mice had significantly more BALF inflammation, which included more total cells, macrophages, and neutrophils, compared with WT mice, and this was abolished by treatment with the GPx mimetic ebselen. BALF inflammation persisted in GPx-1(-/-) mice on Day 10 after infection, and GPx-1(-/-) mice had significantly more influenza-specific CD8(+) T cells in spleen compared with WT mice (n = 3-4; P < 0.05). Infected GPx-1(-/-) mice had greater peribronchial and parenchymal inflammation than WT mice, and viral titer was significantly reduced in GPx-1(-/-) mice at Day 3 (n = 5; P < 0.05). Gene expression analysis revealed that infected GPx-1(-/-) mice had higher whole lung TNF-α, macrophage inflammatory protein (MIP)-1α, MIP-2, KC, and matrix metalloproteinase (MMP)-12 mRNA compared with infected WT mice. GPx-1(-/-) mice had more MIP-2 protein in BALF at Day 3 and more active MMP-9 protease in BALF at Days 3 and 7 than WT mice. These data indicate that GPx-1 reduces influenza A virus-induced lung inflammation.
DOI: 10.1165/rcmb.2011-0345OC
PubMed: 23002098
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000554
- to stream PubMed, to step Curation: 000552
- to stream PubMed, to step Checkpoint: 000526
Links to Exploration step
pubmed:23002098Le document en format XML
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xml:lang="fr"><term>Animaux</term><term>Charge virale</term><term>Espèces réactives de l'oxygène</term><term>Immunité acquise</term><term>Mâle</term><term>Pneumopathie infectieuse</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress caused by excessive reactive oxygen species production is implicated in influenza A virus-induced lung disease. Glutathione peroxidase (GPx)-1 is an antioxidant enzyme that may protect lungs from such damage. The objective of this study was to determine if GPx-1 protects the lung against influenza A virus-induced lung inflammation in vivo. Male wild-type (WT) or GPx-1(-/-) mice were inoculated with HKx31 (H3N2, 1 × 10(4) plaque-forming units), and bronchoalveolar lavage fluid (BALF)/lung compartments were analyzed on Days 3 and 7 after infection for inflammatory marker expression, histology, and viral titer. WT mice infected with HKx31 had significantly more BALF total cells, macrophages, neutrophils, and lymphocytes at Days 3 and 7 compared with naive WT animals (n = 5-8; P < 0.05). However, infected GPx-1(-/-) mice had significantly more BALF inflammation, which included more total cells, macrophages, and neutrophils, compared with WT mice, and this was abolished by treatment with the GPx mimetic ebselen. BALF inflammation persisted in GPx-1(-/-) mice on Day 10 after infection, and GPx-1(-/-) mice had significantly more influenza-specific CD8(+) T cells in spleen compared with WT mice (n = 3-4; P < 0.05). Infected GPx-1(-/-) mice had greater peribronchial and parenchymal inflammation than WT mice, and viral titer was significantly reduced in GPx-1(-/-) mice at Day 3 (n = 5; P < 0.05). Gene expression analysis revealed that infected GPx-1(-/-) mice had higher whole lung TNF-α, macrophage inflammatory protein (MIP)-1α, MIP-2, KC, and matrix metalloproteinase (MMP)-12 mRNA compared with infected WT mice. GPx-1(-/-) mice had more MIP-2 protein in BALF at Day 3 and more active MMP-9 protease in BALF at Days 3 and 7 than WT mice. These data indicate that GPx-1 reduces influenza A virus-induced lung inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23002098</PMID><DateCompleted><Year>2013</Year><Month>02</Month><Day>25</Day></DateCompleted><DateRevised><Year>2013</Year><Month>01</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1535-4989</ISSN><JournalIssue CitedMedium="Internet"><Volume>48</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Jan</Month></PubDate></JournalIssue><Title>American journal of respiratory cell and molecular biology</Title><ISOAbbreviation>Am. J. Respir. Cell Mol. Biol.</ISOAbbreviation></Journal><ArticleTitle>Glutathione peroxidase-1 reduces influenza A virus-induced lung inflammation.</ArticleTitle><Pagination><MedlinePgn>17-26</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2011-0345OC</ELocationID><Abstract><AbstractText>Oxidative stress caused by excessive reactive oxygen species production is implicated in influenza A virus-induced lung disease. Glutathione peroxidase (GPx)-1 is an antioxidant enzyme that may protect lungs from such damage. The objective of this study was to determine if GPx-1 protects the lung against influenza A virus-induced lung inflammation in vivo. Male wild-type (WT) or GPx-1(-/-) mice were inoculated with HKx31 (H3N2, 1 × 10(4) plaque-forming units), and bronchoalveolar lavage fluid (BALF)/lung compartments were analyzed on Days 3 and 7 after infection for inflammatory marker expression, histology, and viral titer. WT mice infected with HKx31 had significantly more BALF total cells, macrophages, neutrophils, and lymphocytes at Days 3 and 7 compared with naive WT animals (n = 5-8; P < 0.05). However, infected GPx-1(-/-) mice had significantly more BALF inflammation, which included more total cells, macrophages, and neutrophils, compared with WT mice, and this was abolished by treatment with the GPx mimetic ebselen. BALF inflammation persisted in GPx-1(-/-) mice on Day 10 after infection, and GPx-1(-/-) mice had significantly more influenza-specific CD8(+) T cells in spleen compared with WT mice (n = 3-4; P < 0.05). Infected GPx-1(-/-) mice had greater peribronchial and parenchymal inflammation than WT mice, and viral titer was significantly reduced in GPx-1(-/-) mice at Day 3 (n = 5; P < 0.05). Gene expression analysis revealed that infected GPx-1(-/-) mice had higher whole lung TNF-α, macrophage inflammatory protein (MIP)-1α, MIP-2, KC, and matrix metalloproteinase (MMP)-12 mRNA compared with infected WT mice. GPx-1(-/-) mice had more MIP-2 protein in BALF at Day 3 and more active MMP-9 protease in BALF at Days 3 and 7 than WT mice. These data indicate that GPx-1 reduces influenza A virus-induced lung inflammation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yatmaz</LastName><ForeName>Selcuk</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, The University of Melbourne, Parkville, VIC, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Seow</LastName><ForeName>Huei Jiunn</ForeName><Initials>HJ</Initials></Author><Author ValidYN="Y"><LastName>Gualano</LastName><ForeName>Rosa C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Wong</LastName><ForeName>Zi Xin</ForeName><Initials>ZX</Initials></Author><Author ValidYN="Y"><LastName>Stambas</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Selemidis</LastName><ForeName>Stavros</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Crack</LastName><ForeName>Peter J</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Bozinovski</LastName><ForeName>Steven</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Gary P</ForeName><Initials>GP</Initials></Author><Author ValidYN="Y"><LastName>Vlahos</LastName><ForeName>Ross</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>09</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Respir Cell Mol Biol</MedlineTA><NlmUniqueID>8917225</NlmUniqueID><ISSNLinking>1044-1549</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001393">Azoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018925">Chemokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016566">Organoselenium Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>40X2P7DPGH</RegistryNumber><NameOfSubstance UI="C042986">ebselen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.-</RegistryNumber><NameOfSubstance UI="C117216">glutathione peroxidase GPX1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.9</RegistryNumber><NameOfSubstance UI="D005979">Glutathione Peroxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.-</RegistryNumber><NameOfSubstance UI="D010447">Peptide Hydrolases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D056704" MajorTopicYN="N">Adaptive Immunity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001393" MajorTopicYN="N">Azoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018925" MajorTopicYN="N">Chemokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005979" MajorTopicYN="N">Glutathione Peroxidase</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053122" MajorTopicYN="Y">Influenza A Virus, H3N2 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016566" MajorTopicYN="N">Organoselenium Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010447" MajorTopicYN="N">Peptide Hydrolases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011014" MajorTopicYN="N">Pneumonia</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>2</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23002098</ArticleId><ArticleId IdType="pii">rcmb.2011-0345OC</ArticleId><ArticleId IdType="doi">10.1165/rcmb.2011-0345OC</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li></country><region><li>Victoria (État)</li></region><settlement><li>Melbourne</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><noCountry><name sortKey="Anderson, Gary P" sort="Anderson, Gary P" uniqKey="Anderson G" first="Gary P" last="Anderson">Gary P. Anderson</name><name sortKey="Bozinovski, Steven" sort="Bozinovski, Steven" uniqKey="Bozinovski S" first="Steven" last="Bozinovski">Steven Bozinovski</name><name sortKey="Crack, Peter J" sort="Crack, Peter J" uniqKey="Crack P" first="Peter J" last="Crack">Peter J. Crack</name><name sortKey="Gualano, Rosa C" sort="Gualano, Rosa C" uniqKey="Gualano R" first="Rosa C" last="Gualano">Rosa C. Gualano</name><name sortKey="Selemidis, Stavros" sort="Selemidis, Stavros" uniqKey="Selemidis S" first="Stavros" last="Selemidis">Stavros Selemidis</name><name sortKey="Seow, Huei Jiunn" sort="Seow, Huei Jiunn" uniqKey="Seow H" first="Huei Jiunn" last="Seow">Huei Jiunn Seow</name><name sortKey="Stambas, John" sort="Stambas, John" uniqKey="Stambas J" first="John" last="Stambas">John Stambas</name><name sortKey="Vlahos, Ross" sort="Vlahos, Ross" uniqKey="Vlahos R" first="Ross" last="Vlahos">Ross Vlahos</name><name sortKey="Wong, Zi Xin" sort="Wong, Zi Xin" uniqKey="Wong Z" first="Zi Xin" last="Wong">Zi Xin Wong</name></noCountry><country name="Australie"><region name="Victoria (État)"><name sortKey="Yatmaz, Selcuk" sort="Yatmaz, Selcuk" uniqKey="Yatmaz S" first="Selcuk" last="Yatmaz">Selcuk Yatmaz</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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