A probable role for IFN-gamma in the development of a lung immunopathology in SARS.
Identifieur interne : 002564 ( PubMed/Corpus ); précédent : 002563; suivant : 002565A probable role for IFN-gamma in the development of a lung immunopathology in SARS.
Auteurs : Michel Theron ; Kao-Jean Huang ; Yu-Wen Chen ; Ching-Chuan Liu ; Huan-Yao LeiSource :
- Cytokine [ 1043-4666 ] ; 2005.
English descriptors
- KwdEn :
- Apoptosis (immunology), Cell Communication (immunology), Cell Cycle (immunology), Cell Line, Tumor, Cell Proliferation, Coronavirus (immunology), Epithelial Cells (metabolism), Epithelial Cells (pathology), Fibroblasts (immunology), Fibroblasts (pathology), Growth Inhibitors (physiology), Humans, Interferon-gamma (physiology), Jurkat Cells, Lung Diseases (immunology), Lung Diseases (metabolism), Lung Diseases (pathology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), fas Receptor (biosynthesis), fas Receptor (genetics), fas Receptor (immunology).
- MESH :
- chemical , biosynthesis : fas Receptor.
- chemical , genetics : fas Receptor.
- chemical , immunology : fas Receptor.
- chemical , physiology : Growth Inhibitors, Interferon-gamma.
- immunology : Apoptosis, Cell Communication, Cell Cycle, Coronavirus, Fibroblasts, Lung Diseases, Severe Acute Respiratory Syndrome.
- metabolism : Epithelial Cells, Lung Diseases, Severe Acute Respiratory Syndrome.
- pathology : Epithelial Cells, Fibroblasts, Lung Diseases, Severe Acute Respiratory Syndrome.
- Cell Line, Tumor, Cell Proliferation, Humans, Jurkat Cells.
Abstract
Recent work carried out in our laboratory showed the existence of a cytokine storm in SARS patients, dominated by Th1-type mediators. We thus hypothesized that IFN-gamma may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-gamma on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-gamma, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-gamma 4--8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-gamma may be responsible for acute lung injury in the late phase of the SARS pathology.
DOI: 10.1016/j.cyto.2005.07.007
PubMed: 16129616
Links to Exploration step
pubmed:16129616Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A probable role for IFN-gamma in the development of a lung immunopathology in SARS.</title><author><name sortKey="Theron, Michel" sort="Theron, Michel" uniqKey="Theron M" first="Michel" last="Theron">Michel Theron</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, 1 Ta-Hsueh Road, Tainan 701, Taiwan.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, Kao Jean" sort="Huang, Kao Jean" uniqKey="Huang K" first="Kao-Jean" last="Huang">Kao-Jean Huang</name></author><author><name sortKey="Chen, Yu Wen" sort="Chen, Yu Wen" uniqKey="Chen Y" first="Yu-Wen" last="Chen">Yu-Wen Chen</name></author><author><name sortKey="Liu, Ching Chuan" sort="Liu, Ching Chuan" uniqKey="Liu C" first="Ching-Chuan" last="Liu">Ching-Chuan Liu</name></author><author><name sortKey="Lei, Huan Yao" sort="Lei, Huan Yao" uniqKey="Lei H" first="Huan-Yao" last="Lei">Huan-Yao Lei</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16129616</idno><idno type="pmid">16129616</idno><idno type="doi">10.1016/j.cyto.2005.07.007</idno><idno type="wicri:Area/PubMed/Corpus">002564</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002564</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A probable role for IFN-gamma in the development of a lung immunopathology in SARS.</title><author><name sortKey="Theron, Michel" sort="Theron, Michel" uniqKey="Theron M" first="Michel" last="Theron">Michel Theron</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, 1 Ta-Hsueh Road, Tainan 701, Taiwan.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, Kao Jean" sort="Huang, Kao Jean" uniqKey="Huang K" first="Kao-Jean" last="Huang">Kao-Jean Huang</name></author><author><name sortKey="Chen, Yu Wen" sort="Chen, Yu Wen" uniqKey="Chen Y" first="Yu-Wen" last="Chen">Yu-Wen Chen</name></author><author><name sortKey="Liu, Ching Chuan" sort="Liu, Ching Chuan" uniqKey="Liu C" first="Ching-Chuan" last="Liu">Ching-Chuan Liu</name></author><author><name sortKey="Lei, Huan Yao" sort="Lei, Huan Yao" uniqKey="Lei H" first="Huan-Yao" last="Lei">Huan-Yao Lei</name></author></analytic><series><title level="j">Cytokine</title><idno type="ISSN">1043-4666</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (immunology)</term><term>Cell Communication (immunology)</term><term>Cell Cycle (immunology)</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Coronavirus (immunology)</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (pathology)</term><term>Fibroblasts (immunology)</term><term>Fibroblasts (pathology)</term><term>Growth Inhibitors (physiology)</term><term>Humans</term><term>Interferon-gamma (physiology)</term><term>Jurkat Cells</term><term>Lung Diseases (immunology)</term><term>Lung Diseases (metabolism)</term><term>Lung Diseases (pathology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>fas Receptor (biosynthesis)</term><term>fas Receptor (genetics)</term><term>fas Receptor (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Growth Inhibitors</term><term>Interferon-gamma</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Apoptosis</term><term>Cell Communication</term><term>Cell Cycle</term><term>Coronavirus</term><term>Fibroblasts</term><term>Lung Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Lung Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Epithelial Cells</term><term>Fibroblasts</term><term>Lung Diseases</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Humans</term><term>Jurkat Cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent work carried out in our laboratory showed the existence of a cytokine storm in SARS patients, dominated by Th1-type mediators. We thus hypothesized that IFN-gamma may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-gamma on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-gamma, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-gamma 4--8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-gamma may be responsible for acute lung injury in the late phase of the SARS pathology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16129616</PMID><DateCompleted><Year>2008</Year><Month>06</Month><Day>03</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1043-4666</ISSN><JournalIssue CitedMedium="Print"><Volume>32</Volume><Issue>1</Issue><PubDate><Year>2005</Year><Month>Oct</Month><Day>07</Day></PubDate></JournalIssue><Title>Cytokine</Title><ISOAbbreviation>Cytokine</ISOAbbreviation></Journal><ArticleTitle>A probable role for IFN-gamma in the development of a lung immunopathology in SARS.</ArticleTitle><Pagination><MedlinePgn>30-8</MedlinePgn></Pagination><Abstract><AbstractText>Recent work carried out in our laboratory showed the existence of a cytokine storm in SARS patients, dominated by Th1-type mediators. We thus hypothesized that IFN-gamma may play a major role in the pathology by triggering immune-mediated alveolar damage. As we assessed or re-assessed some effects of IFN-gamma on a number of human lung epithelial and fibroblast cell lines, chosen for their wide use in the literature, we found that alveolar epithelial cells were more sensitive to IFN-gamma, in terms of proliferation inhibition and enhancement of Fas-mediated apoptosis. While similar effects were obtained on fibroblasts, concentrations of IFN-gamma 4--8-fold greater were required. In addition, both epithelial and fibroblastic cell lines were able to secrete large quantities of T cell-targeting chemokines, similar to the ones detected in SARS patients. Based on the clinical data collected previously, the available literature and our in vitro experimentation, we propose that IFN-gamma may be responsible for acute lung injury in the late phase of the SARS pathology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Theron</LastName><ForeName>Michel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, 1 Ta-Hsueh Road, Tainan 701, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Kao-Jean</ForeName><Initials>KJ</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yu-Wen</ForeName><Initials>YW</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ching-Chuan</ForeName><Initials>CC</Initials></Author><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Huan-Yao</ForeName><Initials>HY</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cytokine</MedlineTA><NlmUniqueID>9005353</NlmUniqueID><ISSNLinking>1043-4666</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006131">Growth Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019014">fas Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000276" 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MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006131" MajorTopicYN="N">Growth Inhibitors</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019169" MajorTopicYN="N">Jurkat Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008171" MajorTopicYN="N">Lung Diseases</DescriptorName><QualifierName UI="Q000276" 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