Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.
Identifieur interne : 002552 ( Main/Exploration ); précédent : 002551; suivant : 002553Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.
Auteurs : Tomoki Yoshikawa [États-Unis] ; Terence E. Hill ; Naoko Yoshikawa ; Vsevolod L. Popov ; Cristi L. Galindo ; Harold R. Garner ; C J Peters ; Chien-Te Kent TsengSource :
- PloS one [ 1932-6203 ] ; 2010.
Descripteurs français
- KwdFr :
- Bronches (cytologie), Bronches (immunologie), Cellules cultivées, Cellules épithéliales (immunologie), Expression des gènes, Facteur de transcription NF-kappa B (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Facteur-7 de régulation d'interféron (métabolisme), Humains, Immunité innée, Réplication virale, Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (génétique), Virus du SRAS (physiologie).
- MESH :
- cytologie : Bronches.
- génétique : Virus du SRAS.
- immunologie : Bronches, Cellules épithéliales, Syndrome respiratoire aigu sévère.
- métabolisme : Facteur de transcription NF-kappa B, Facteur-3 de régulation d'interféron, Facteur-7 de régulation d'interféron.
- physiologie : Virus du SRAS.
- Cellules cultivées, Expression des gènes, Humains, Immunité innée, Réplication virale.
English descriptors
- KwdEn :
- Bronchi (cytology), Bronchi (immunology), Cells, Cultured, Epithelial Cells (immunology), Gene Expression, Humans, Immunity, Innate, Interferon Regulatory Factor-3 (metabolism), Interferon Regulatory Factor-7 (metabolism), NF-kappa B (metabolism), SARS Virus (genetics), SARS Virus (physiology), Severe Acute Respiratory Syndrome (immunology), Virus Replication.
- MESH :
- chemical , metabolism : Interferon Regulatory Factor-3, Interferon Regulatory Factor-7, NF-kappa B.
- cytology : Bronchi.
- genetics : SARS Virus.
- immunology : Bronchi, Epithelial Cells, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- Cells, Cultured, Gene Expression, Humans, Immunity, Innate, Virus Replication.
Abstract
Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome-associated coronavirus (SARS-CoV). Not only can these cells support the growth of SARS-CoV infection, but they are also capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelial signaling to SARS-CoV is crucial for paving the way to better understand SARS pathogenesis. Based on microarray-based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derived from Calu-3 cells. Specifically, we found a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1, and interferon regulatory factor (IRF)-3/7 in infected 2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.), resulting in the activation of many antiviral genes, including interferon (IFN)-beta, -lambdas, inflammatory mediators, and many IFN-stimulated genes (ISGs). We also showed, for the first time, that IFN-beta and IFN-lambdas were capable of exerting previously unrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detected in infected 2B4 bronchial epithelial cells until 48 hrs p.i. Collectively, our results highlight the mechanics of the sequential events of antiviral signaling pathway/s triggered by SARS-CoV in bronchial epithelial cells and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.
DOI: 10.1371/journal.pone.0008729
PubMed: 20090954
Affiliations:
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Le document en format XML
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Hill</name></author><author><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name></author><author><name sortKey="Popov, Vsevolod L" sort="Popov, Vsevolod L" uniqKey="Popov V" first="Vsevolod L" last="Popov">Vsevolod L. Popov</name></author><author><name sortKey="Galindo, Cristi L" sort="Galindo, Cristi L" uniqKey="Galindo C" first="Cristi L" last="Galindo">Cristi L. Galindo</name></author><author><name sortKey="Garner, Harold R" sort="Garner, Harold R" uniqKey="Garner H" first="Harold R" last="Garner">Harold R. Garner</name></author><author><name sortKey="Peters, C J" sort="Peters, C J" uniqKey="Peters C" first="C J" last="Peters">C J Peters</name></author><author><name sortKey="Tseng, Chien Te Kent" sort="Tseng, Chien Te Kent" uniqKey="Tseng C" first="Chien-Te Kent" last="Tseng">Chien-Te Kent Tseng</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20090954</idno><idno type="pmid">20090954</idno><idno type="doi">10.1371/journal.pone.0008729</idno><idno type="wicri:Area/PubMed/Corpus">001764</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001764</idno><idno type="wicri:Area/PubMed/Curation">001764</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001764</idno><idno type="wicri:Area/PubMed/Checkpoint">001687</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001687</idno><idno type="wicri:Area/Ncbi/Merge">002063</idno><idno type="wicri:Area/Ncbi/Curation">002063</idno><idno type="wicri:Area/Ncbi/Checkpoint">002063</idno><idno type="wicri:Area/Main/Merge">002590</idno><idno type="wicri:Area/Main/Curation">002552</idno><idno type="wicri:Area/Main/Exploration">002552</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.</title><author><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, United States of America.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Hill, Terence E" sort="Hill, Terence E" uniqKey="Hill T" first="Terence E" last="Hill">Terence E. Hill</name></author><author><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name></author><author><name sortKey="Popov, Vsevolod L" sort="Popov, Vsevolod L" uniqKey="Popov V" first="Vsevolod L" last="Popov">Vsevolod L. Popov</name></author><author><name sortKey="Galindo, Cristi L" sort="Galindo, Cristi L" uniqKey="Galindo C" first="Cristi L" last="Galindo">Cristi L. Galindo</name></author><author><name sortKey="Garner, Harold R" sort="Garner, Harold R" uniqKey="Garner H" first="Harold R" last="Garner">Harold R. Garner</name></author><author><name sortKey="Peters, C J" sort="Peters, C J" uniqKey="Peters C" first="C J" last="Peters">C J Peters</name></author><author><name sortKey="Tseng, Chien Te Kent" sort="Tseng, Chien Te Kent" uniqKey="Tseng C" first="Chien-Te Kent" last="Tseng">Chien-Te Kent Tseng</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bronchi (cytology)</term><term>Bronchi (immunology)</term><term>Cells, Cultured</term><term>Epithelial Cells (immunology)</term><term>Gene Expression</term><term>Humans</term><term>Immunity, Innate</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Interferon Regulatory Factor-7 (metabolism)</term><term>NF-kappa B (metabolism)</term><term>SARS Virus (genetics)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Bronches (cytologie)</term><term>Bronches (immunologie)</term><term>Cellules cultivées</term><term>Cellules épithéliales (immunologie)</term><term>Expression des gènes</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Facteur-7 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Immunité innée</term><term>Réplication virale</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Interferon Regulatory Factor-7</term><term>NF-kappa B</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Bronches</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bronchi</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Bronches</term><term>Cellules épithéliales</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Bronchi</term><term>Epithelial Cells</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term><term>Facteur-3 de régulation d'interféron</term><term>Facteur-7 de régulation d'interféron</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Gene Expression</term><term>Humans</term><term>Immunity, Innate</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Expression des gènes</term><term>Humains</term><term>Immunité innée</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome-associated coronavirus (SARS-CoV). Not only can these cells support the growth of SARS-CoV infection, but they are also capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelial signaling to SARS-CoV is crucial for paving the way to better understand SARS pathogenesis. Based on microarray-based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derived from Calu-3 cells. Specifically, we found a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1, and interferon regulatory factor (IRF)-3/7 in infected 2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.), resulting in the activation of many antiviral genes, including interferon (IFN)-beta, -lambdas, inflammatory mediators, and many IFN-stimulated genes (ISGs). We also showed, for the first time, that IFN-beta and IFN-lambdas were capable of exerting previously unrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detected in infected 2B4 bronchial epithelial cells until 48 hrs p.i. Collectively, our results highlight the mechanics of the sequential events of antiviral signaling pathway/s triggered by SARS-CoV in bronchial epithelial cells and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><noCountry><name sortKey="Galindo, Cristi L" sort="Galindo, Cristi L" uniqKey="Galindo C" first="Cristi L" last="Galindo">Cristi L. Galindo</name><name sortKey="Garner, Harold R" sort="Garner, Harold R" uniqKey="Garner H" first="Harold R" last="Garner">Harold R. Garner</name><name sortKey="Hill, Terence E" sort="Hill, Terence E" uniqKey="Hill T" first="Terence E" last="Hill">Terence E. Hill</name><name sortKey="Peters, C J" sort="Peters, C J" uniqKey="Peters C" first="C J" last="Peters">C J Peters</name><name sortKey="Popov, Vsevolod L" sort="Popov, Vsevolod L" uniqKey="Popov V" first="Vsevolod L" last="Popov">Vsevolod L. Popov</name><name sortKey="Tseng, Chien Te Kent" sort="Tseng, Chien Te Kent" uniqKey="Tseng C" first="Chien-Te Kent" last="Tseng">Chien-Te Kent Tseng</name><name sortKey="Yoshikawa, Naoko" sort="Yoshikawa, Naoko" uniqKey="Yoshikawa N" first="Naoko" last="Yoshikawa">Naoko Yoshikawa</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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