SARS-CoV virus-host interactions and comparative etiologies of acute respiratory distress syndrome as determined by transcriptional and cytokine profiling of formalin-fixed paraffin-embedded tissues.
Identifieur interne : 002019 ( PubMed/Checkpoint ); précédent : 002018; suivant : 002020SARS-CoV virus-host interactions and comparative etiologies of acute respiratory distress syndrome as determined by transcriptional and cytokine profiling of formalin-fixed paraffin-embedded tissues.
Auteurs : Tracey Baas [États-Unis] ; Jeffery K. Taubenberger ; Pek Yoon Chong ; Paul Chui ; Michael G. KatzeSource :
- Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research [ 1079-9907 ] ; 2006.
Descripteurs français
- KwdFr :
- Adulte d'âge moyen, Analyse de profil d'expression de gènes, Autopsie, Cytokines (génétique), Femelle, Formaldéhyde, Humains, Inclusion en paraffine, Interactions hôte-parasite, Mâle, Nourrisson, Sujet âgé, Sujet âgé de 80 ans ou plus, Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Transcription génétique (génétique), Transduction du signal, Virus du SRAS (physiologie).
- MESH :
- génétique : Cytokines, Syndrome respiratoire aigu sévère, Transcription génétique.
- immunologie : Syndrome respiratoire aigu sévère.
- métabolisme : Syndrome respiratoire aigu sévère.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Adulte d'âge moyen, Analyse de profil d'expression de gènes, Autopsie, Femelle, Formaldéhyde, Humains, Inclusion en paraffine, Interactions hôte-parasite, Mâle, Nourrisson, Sujet âgé, Sujet âgé de 80 ans ou plus, Transduction du signal.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Autopsy, Cytokines (genetics), Female, Formaldehyde, Gene Expression Profiling, Host-Parasite Interactions, Humans, Infant, Male, Middle Aged, Paraffin Embedding, SARS Virus (physiology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Signal Transduction, Transcription, Genetic (genetics).
- MESH :
- chemical , genetics : Cytokines.
- genetics : Severe Acute Respiratory Syndrome, Transcription, Genetic.
- immunology : Severe Acute Respiratory Syndrome.
- metabolism : Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Aged, Aged, 80 and over, Autopsy, Female, Formaldehyde, Gene Expression Profiling, Host-Parasite Interactions, Humans, Infant, Male, Middle Aged, Paraffin Embedding, Signal Transduction.
Abstract
These studies attempt to understand more fully the host response and pathogenesis associated with severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) by monitoring gene expression using formalin-fixed paraffin-embedded (FFPE) pulmonary autopsy tissues. These tissues were from patients in different hospitals in Singapore who were diagnosed with various microbial infections, including SARS-CoV, that caused acute respiratory distress syndrome (ARDS). Global expression patterns showed limited correlation between end-stage ARDS and the initiating pathogen, but when focusing on a subset of genes implicated in pulmonary pathogenesis, molecular signatures of pulmonary disease were obtained and appeared to be influenced by preexisting pulmonary complications and also bacterial components of infection. Many factors detected during pulmonary damage and repair, such as extracellular matrix (ECM) components, transforming growth factor (TGF) enhancers, acute-phase proteins, and antioxidants, were included in the molecular profiles of these ARDS lung tissues. In addition, differential expression of cytokines within these pulmonary tissues were observed, including notable genes involved in the interferon (IFN) pathway, such as Stat1, IFN regulatory factor-1 (IRF-1), interleukin-6 (IL-6), IL-8, and IL-18, that are often characterized as elevated in ARDS patients.
DOI: 10.1089/jir.2006.26.309
PubMed: 16689659
Affiliations:
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These tissues were from patients in different hospitals in Singapore who were diagnosed with various microbial infections, including SARS-CoV, that caused acute respiratory distress syndrome (ARDS). Global expression patterns showed limited correlation between end-stage ARDS and the initiating pathogen, but when focusing on a subset of genes implicated in pulmonary pathogenesis, molecular signatures of pulmonary disease were obtained and appeared to be influenced by preexisting pulmonary complications and also bacterial components of infection. Many factors detected during pulmonary damage and repair, such as extracellular matrix (ECM) components, transforming growth factor (TGF) enhancers, acute-phase proteins, and antioxidants, were included in the molecular profiles of these ARDS lung tissues. In addition, differential expression of cytokines within these pulmonary tissues were observed, including notable genes involved in the interferon (IFN) pathway, such as Stat1, IFN regulatory factor-1 (IRF-1), interleukin-6 (IL-6), IL-8, and IL-18, that are often characterized as elevated in ARDS patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16689659</PMID><DateCompleted><Year>2007</Year><Month>04</Month><Day>24</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1079-9907</ISSN><JournalIssue CitedMedium="Print"><Volume>26</Volume><Issue>5</Issue><PubDate><Year>2006</Year><Month>May</Month></PubDate></JournalIssue><Title>Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research</Title><ISOAbbreviation>J. Interferon Cytokine Res.</ISOAbbreviation></Journal><ArticleTitle>SARS-CoV virus-host interactions and comparative etiologies of acute respiratory distress syndrome as determined by transcriptional and cytokine profiling of formalin-fixed paraffin-embedded tissues.</ArticleTitle><Pagination><MedlinePgn>309-17</MedlinePgn></Pagination><Abstract><AbstractText>These studies attempt to understand more fully the host response and pathogenesis associated with severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) by monitoring gene expression using formalin-fixed paraffin-embedded (FFPE) pulmonary autopsy tissues. These tissues were from patients in different hospitals in Singapore who were diagnosed with various microbial infections, including SARS-CoV, that caused acute respiratory distress syndrome (ARDS). Global expression patterns showed limited correlation between end-stage ARDS and the initiating pathogen, but when focusing on a subset of genes implicated in pulmonary pathogenesis, molecular signatures of pulmonary disease were obtained and appeared to be influenced by preexisting pulmonary complications and also bacterial components of infection. Many factors detected during pulmonary damage and repair, such as extracellular matrix (ECM) components, transforming growth factor (TGF) enhancers, acute-phase proteins, and antioxidants, were included in the molecular profiles of these ARDS lung tissues. In addition, differential expression of cytokines within these pulmonary tissues were observed, including notable genes involved in the interferon (IFN) pathway, such as Stat1, IFN regulatory factor-1 (IRF-1), interleukin-6 (IL-6), IL-8, and IL-18, that are often characterized as elevated in ARDS patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baas</LastName><ForeName>Tracey</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Microbiology, School of Medicine, University of Washington, Seattle, WA 98195, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taubenberger</LastName><ForeName>Jeffery K</ForeName><Initials>JK</Initials></Author><Author ValidYN="Y"><LastName>Chong</LastName><ForeName>Pek Yoon</ForeName><Initials>PY</Initials></Author><Author ValidYN="Y"><LastName>Chui</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AI052106</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AI058113</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Z01 AI000986-01</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51RR00166</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51 RR000166</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><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><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Interferon Cytokine Res</MedlineTA><NlmUniqueID>9507088</NlmUniqueID><ISSNLinking>1079-9907</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>1HG84L3525</RegistryNumber><NameOfSubstance UI="D005557">Formaldehyde</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001344" MajorTopicYN="N">Autopsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005557" MajorTopicYN="N">Formaldehyde</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="Y">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006790" MajorTopicYN="N">Host-Parasite Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016612" MajorTopicYN="N">Paraffin Embedding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName><QualifierName UI="Q000235" 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Aug;59(1-3):118-28</Citation><ArticleIdList><ArticleId IdType="pubmed">24845462</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="Chong, Pek Yoon" sort="Chong, Pek Yoon" uniqKey="Chong P" first="Pek Yoon" last="Chong">Pek Yoon Chong</name><name sortKey="Chui, Paul" sort="Chui, Paul" uniqKey="Chui P" first="Paul" last="Chui">Paul Chui</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K" last="Taubenberger">Jeffery K. Taubenberger</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Baas, Tracey" sort="Baas, Tracey" uniqKey="Baas T" first="Tracey" last="Baas">Tracey Baas</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= SARS-CoV virus-host interactions and comparative etiologies of acute respiratory distress syndrome as determined by transcriptional and cytokine profiling of formalin-fixed paraffin-embedded tissues.
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Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:16689659" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
| This area was generated with Dilib version V0.6.33. |  |