Exacerbated innate host response to SARS-CoV in aged non-human primates.
Identifieur interne : 002539 ( Main/Exploration ); précédent : 002538; suivant : 002540Exacerbated 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
Affiliations:
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Smits</name><affiliation wicri:level="3"><nlm:affiliation>Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Virology, Erasmus Medical Center, Rotterdam</wicri:regionArea><placeName><settlement type="city">Rotterdam</settlement><region nuts="2" type="province">Hollande-Méridionale</region></placeName></affiliation></author><author><name sortKey="De Lang, Anna" sort="De Lang, Anna" uniqKey="De Lang A" first="Anna" last="De Lang">Anna De Lang</name></author><author><name sortKey="Van Den Brand, Judith M A" sort="Van Den Brand, Judith M A" uniqKey="Van Den Brand J" first="Judith M A" last="Van Den Brand">Judith M A. Van Den Brand</name></author><author><name sortKey="Leijten, Lonneke M" sort="Leijten, Lonneke M" uniqKey="Leijten L" first="Lonneke M" last="Leijten">Lonneke M. Leijten</name></author><author><name sortKey="Van Ijcken, Wilfred F" sort="Van Ijcken, Wilfred F" uniqKey="Van Ijcken W" first="Wilfred F" last="Van Ijcken">Wilfred F. Van Ijcken</name></author><author><name sortKey="Eijkemans, Marinus J C" sort="Eijkemans, Marinus J C" uniqKey="Eijkemans M" first="Marinus J C" last="Eijkemans">Marinus J C. Eijkemans</name></author><author><name sortKey="Van Amerongen, Geert" sort="Van Amerongen, Geert" uniqKey="Van Amerongen G" first="Geert" last="Van Amerongen">Geert Van Amerongen</name></author><author><name sortKey="Kuiken, Thijs" sort="Kuiken, Thijs" uniqKey="Kuiken T" first="Thijs" last="Kuiken">Thijs Kuiken</name></author><author><name sortKey="Andeweg, Arno C" sort="Andeweg, Arno C" uniqKey="Andeweg A" first="Arno C" last="Andeweg">Arno C. Andeweg</name></author><author><name sortKey="Osterhaus, Albert D M E" sort="Osterhaus, Albert D M E" uniqKey="Osterhaus A" first="Albert D M E" last="Osterhaus">Albert D M E. 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Haagmans</name></author></analytic><series><title level="j">PLoS pathogens</title><idno type="eISSN">1553-7374</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (immunology)</term><term>Acute Lung Injury (virology)</term><term>Aging (immunology)</term><term>Animals</term><term>Anti-Inflammatory Agents (pharmacology)</term><term>Gene Expression</term><term>Gene Expression Profiling</term><term>Immunity, Innate (immunology)</term><term>Immunohistochemistry</term><term>Inflammation (immunology)</term><term>Interferon Type I (biosynthesis)</term><term>Interferon Type I (immunology)</term><term>Interferon Type I (pharmacology)</term><term>Interleukin-8 (immunology)</term><term>Macaca</term><term>NF-kappa B (biosynthesis)</term><term>NF-kappa B (immunology)</term><term>Oligonucleotide Array Sequence Analysis</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Signal Transduction (immunology)</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Anti-inflammatoires (pharmacologie)</term><term>Expression des gènes</term><term>Facteur de transcription NF-kappa B (biosynthèse)</term><term>Facteur de transcription NF-kappa B (immunologie)</term><term>Immunité innée (immunologie)</term><term>Immunohistochimie</term><term>Inflammation (immunologie)</term><term>Interféron de type I (biosynthèse)</term><term>Interféron de type I (immunologie)</term><term>Interféron de type I (pharmacologie)</term><term>Interleukine-8 (immunologie)</term><term>Lésion pulmonaire aigüe (immunologie)</term><term>Lésion pulmonaire aigüe (virologie)</term><term>Macaca</term><term>RT-PCR</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Séquençage par oligonucléotides en batterie</term><term>Transduction du signal (immunologie)</term><term>Vieillissement (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon Type I</term><term>NF-kappa B</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Type I</term><term>Interleukin-8</term><term>NF-kappa B</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term><term>Immunité innée</term><term>Inflammation</term><term>Interféron de type I</term><term>Interleukine-8</term><term>Lésion pulmonaire aigüe</term><term>Syndrome respiratoire aigu sévère</term><term>Transduction du signal</term><term>Vieillissement</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Acute Lung Injury</term><term>Aging</term><term>Immunity, Innate</term><term>Inflammation</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Acute Lung Injury</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression</term><term>Gene Expression Profiling</term><term>Immunohistochemistry</term><term>Macaca</term><term>Oligonucleotide Array Sequence Analysis</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Expression des gènes</term><term>Immunohistochimie</term><term>Macaca</term><term>RT-PCR</term><term>Réplication virale</term><term>Séquençage par oligonucléotides en batterie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li></country><region><li>Hollande-Méridionale</li></region><settlement><li>Rotterdam</li></settlement></list><tree><noCountry><name sortKey="Andeweg, Arno C" sort="Andeweg, Arno C" uniqKey="Andeweg A" first="Arno C" last="Andeweg">Arno C. Andeweg</name><name sortKey="De Lang, Anna" sort="De Lang, Anna" uniqKey="De Lang A" first="Anna" last="De Lang">Anna De Lang</name><name sortKey="Eijkemans, Marinus J C" sort="Eijkemans, Marinus J C" uniqKey="Eijkemans M" first="Marinus J C" last="Eijkemans">Marinus J C. Eijkemans</name><name sortKey="Haagmans, Bart L" sort="Haagmans, Bart L" uniqKey="Haagmans B" first="Bart L" last="Haagmans">Bart L. Haagmans</name><name sortKey="Kuiken, Thijs" sort="Kuiken, Thijs" uniqKey="Kuiken T" first="Thijs" last="Kuiken">Thijs Kuiken</name><name sortKey="Leijten, Lonneke M" sort="Leijten, Lonneke M" uniqKey="Leijten L" first="Lonneke M" last="Leijten">Lonneke M. Leijten</name><name sortKey="Osterhaus, Albert D M E" sort="Osterhaus, Albert D M E" uniqKey="Osterhaus A" first="Albert D M E" last="Osterhaus">Albert D M E. Osterhaus</name><name sortKey="Van Amerongen, Geert" sort="Van Amerongen, Geert" uniqKey="Van Amerongen G" first="Geert" last="Van Amerongen">Geert Van Amerongen</name><name sortKey="Van Den Brand, Judith M A" sort="Van Den Brand, Judith M A" uniqKey="Van Den Brand J" first="Judith M A" last="Van Den Brand">Judith M A. Van Den Brand</name><name sortKey="Van Ijcken, Wilfred F" sort="Van Ijcken, Wilfred F" uniqKey="Van Ijcken W" first="Wilfred F" last="Van Ijcken">Wilfred F. Van Ijcken</name></noCountry><country name="Pays-Bas"><region name="Hollande-Méridionale"><name sortKey="Smits, Saskia L" sort="Smits, Saskia L" uniqKey="Smits S" first="Saskia L" last="Smits">Saskia L. Smits</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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