Exacerbated innate host response to SARS-CoV in aged non-human primates.
Identifieur interne : 002072 ( Ncbi/Merge ); précédent : 002071; suivant : 002073Exacerbated innate host response to SARS-CoV in aged non-human primates.
Auteurs : Saskia L. Smits [Pays-Bas] ; Anna De Lang ; Judith M A. Van Den Brand ; Lonneke M. Leijten ; Wilfred F. Van Ijcken ; Marinus J C. Eijkemans ; Geert Van Amerongen ; Thijs Kuiken ; Arno C. Andeweg ; Albert D M E. Osterhaus ; Bart L. HaagmansSource :
- PLoS pathogens [ 1553-7374 ] ; 2010.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Animaux, Anti-inflammatoires (pharmacologie), Expression des gènes, Facteur de transcription NF-kappa B (biosynthèse), Facteur de transcription NF-kappa B (immunologie), Immunité innée (immunologie), Immunohistochimie, Inflammation (immunologie), Interféron de type I (biosynthèse), Interféron de type I (immunologie), Interféron de type I (pharmacologie), Interleukine-8 (immunologie), Lésion pulmonaire aigüe (immunologie), Lésion pulmonaire aigüe (virologie), Macaca, RT-PCR, Réplication virale, Syndrome respiratoire aigu sévère (immunologie), Séquençage par oligonucléotides en batterie, Transduction du signal (immunologie), Vieillissement (immunologie), Virus du SRAS (immunologie).
- MESH :
- biosynthèse : Facteur de transcription NF-kappa B, Interféron de type I.
- immunologie : Facteur de transcription NF-kappa B, Immunité innée, Inflammation, Interféron de type I, Interleukine-8, Lésion pulmonaire aigüe, Syndrome respiratoire aigu sévère, Transduction du signal, Vieillissement, Virus du SRAS.
- pharmacologie : Anti-inflammatoires, Interféron de type I.
- virologie : Lésion pulmonaire aigüe.
- Analyse de profil d'expression de gènes, Animaux, Expression des gènes, Immunohistochimie, Macaca, RT-PCR, Réplication virale, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Acute Lung Injury (immunology), Acute Lung Injury (virology), Aging (immunology), Animals, Anti-Inflammatory Agents (pharmacology), Gene Expression, Gene Expression Profiling, Immunity, Innate (immunology), Immunohistochemistry, Inflammation (immunology), Interferon Type I (biosynthesis), Interferon Type I (immunology), Interferon Type I (pharmacology), Interleukin-8 (immunology), Macaca, NF-kappa B (biosynthesis), NF-kappa B (immunology), Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Signal Transduction (immunology), Virus Replication.
- MESH :
- chemical , biosynthesis : Interferon Type I, NF-kappa B.
- chemical , immunology : Interferon Type I, Interleukin-8, NF-kappa B.
- chemical , pharmacology : Anti-Inflammatory Agents, Interferon Type I.
- immunology : Acute Lung Injury, Aging, Immunity, Innate, Inflammation, SARS Virus, Severe Acute Respiratory Syndrome, Signal Transduction.
- virology : Acute Lung Injury.
- Animals, Gene Expression, Gene Expression Profiling, Immunohistochemistry, Macaca, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Virus Replication.
Abstract
The emergence of viral respiratory pathogens with pandemic potential, such as severe acute respiratory syndrome coronavirus (SARS-CoV) and influenza A H5N1, urges the need for deciphering their pathogenesis to develop new intervention strategies. SARS-CoV infection causes acute lung injury (ALI) that may develop into life-threatening acute respiratory distress syndrome (ARDS) with advanced age correlating positively with adverse disease outcome. The molecular pathways, however, that cause virus-induced ALI/ARDS in aged individuals are ill-defined. Here, we show that SARS-CoV-infected aged macaques develop more severe pathology than young adult animals, even though viral replication levels are similar. Comprehensive genomic analyses indicate that aged macaques have a stronger host response to virus infection than young adult macaques, with an increase in differential expression of genes associated with inflammation, with NF-kappaB as central player, whereas expression of type I interferon (IFN)-beta is reduced. Therapeutic treatment of SARS-CoV-infected aged macaques with type I IFN reduces pathology and diminishes pro-inflammatory gene expression, including interleukin-8 (IL-8) levels, without affecting virus replication in the lungs. Thus, ALI in SARS-CoV-infected aged macaques developed as a result of an exacerbated innate host response. The anti-inflammatory action of type I IFN reveals a potential intervention strategy for virus-induced ALI.
DOI: 10.1371/journal.ppat.1000756
PubMed: 20140198
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pubmed:20140198Le document en format XML
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SARS-CoV infection causes acute lung injury (ALI) that may develop into life-threatening acute respiratory distress syndrome (ARDS) with advanced age correlating positively with adverse disease outcome. The molecular pathways, however, that cause virus-induced ALI/ARDS in aged individuals are ill-defined. Here, we show that SARS-CoV-infected aged macaques develop more severe pathology than young adult animals, even though viral replication levels are similar. Comprehensive genomic analyses indicate that aged macaques have a stronger host response to virus infection than young adult macaques, with an increase in differential expression of genes associated with inflammation, with NF-kappaB as central player, whereas expression of type I interferon (IFN)-beta is reduced. Therapeutic treatment of SARS-CoV-infected aged macaques with type I IFN reduces pathology and diminishes pro-inflammatory gene expression, including interleukin-8 (IL-8) levels, without affecting virus replication in the lungs. Thus, ALI in SARS-CoV-infected aged macaques developed as a result of an exacerbated innate host response. The anti-inflammatory action of type I IFN reveals a potential intervention strategy for virus-induced ALI.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20140198</PMID><DateCompleted><Year>2010</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1553-7374</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>2</Issue><PubDate><Year>2010</Year><Month>Feb</Month><Day>05</Day></PubDate></JournalIssue><Title>PLoS pathogens</Title><ISOAbbreviation>PLoS Pathog.</ISOAbbreviation></Journal><ArticleTitle>Exacerbated innate host response to SARS-CoV in aged non-human primates.</ArticleTitle><Pagination><MedlinePgn>e1000756</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.ppat.1000756</ELocationID><Abstract><AbstractText>The emergence of viral respiratory pathogens with pandemic potential, such as severe acute respiratory syndrome coronavirus (SARS-CoV) and influenza A H5N1, urges the need for deciphering their pathogenesis to develop new intervention strategies. SARS-CoV infection causes acute lung injury (ALI) that may develop into life-threatening acute respiratory distress syndrome (ARDS) with advanced age correlating positively with adverse disease outcome. The molecular pathways, however, that cause virus-induced ALI/ARDS in aged individuals are ill-defined. Here, we show that SARS-CoV-infected aged macaques develop more severe pathology than young adult animals, even though viral replication levels are similar. Comprehensive genomic analyses indicate that aged macaques have a stronger host response to virus infection than young adult macaques, with an increase in differential expression of genes associated with inflammation, with NF-kappaB as central player, whereas expression of type I interferon (IFN)-beta is reduced. Therapeutic treatment of SARS-CoV-infected aged macaques with type I IFN reduces pathology and diminishes pro-inflammatory gene expression, including interleukin-8 (IL-8) levels, without affecting virus replication in the lungs. Thus, ALI in SARS-CoV-infected aged macaques developed as a result of an exacerbated innate host response. The anti-inflammatory action of type I IFN reveals a potential intervention strategy for virus-induced ALI.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Smits</LastName><ForeName>Saskia L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Lang</LastName><ForeName>Anna</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>van den Brand</LastName><ForeName>Judith M A</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Leijten</LastName><ForeName>Lonneke M</ForeName><Initials>LM</Initials></Author><Author ValidYN="Y"><LastName>van IJcken</LastName><ForeName>Wilfred F</ForeName><Initials>WF</Initials></Author><Author ValidYN="Y"><LastName>Eijkemans</LastName><ForeName>Marinus J C</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>van Amerongen</LastName><ForeName>Geert</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Kuiken</LastName><ForeName>Thijs</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Andeweg</LastName><ForeName>Arno C</ForeName><Initials>AC</Initials></Author><Author ValidYN="Y"><LastName>Osterhaus</LastName><ForeName>Albert D M E</ForeName><Initials>AD</Initials></Author><Author ValidYN="Y"><LastName>Haagmans</LastName><ForeName>Bart L</ForeName><Initials>BL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL080621</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL080621-01A1</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>02</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Pathog</MedlineTA><NlmUniqueID>101238921</NlmUniqueID><ISSNLinking>1553-7366</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016209">Interleukin-8</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D055371" MajorTopicYN="N">Acute Lung Injury</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName 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MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000276" 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