Innate immune response of human alveolar type II cells infected with severe acute respiratory syndrome-coronavirus.
Identifieur interne : 001910 ( Main/Exploration ); précédent : 001909; suivant : 001911Innate immune response of human alveolar type II cells infected with severe acute respiratory syndrome-coronavirus.
Auteurs : Zhaohui Qian [États-Unis] ; Emily A. Travanty ; Lauren Oko ; Karen Edeen ; Andrew Berglund ; Jieru Wang ; Yoko Ito ; Kathryn V. Holmes ; Robert J. MasonSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2013.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Alvéoles pulmonaires (cytologie), Alvéoles pulmonaires (immunologie), Alvéoles pulmonaires (virologie), Antigènes viraux (immunologie), Antigènes viraux (métabolisme), Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Culture primaire de cellules, Cytoplasme (immunologie), Cytoplasme (ultrastructure), Cytoplasme (virologie), Différenciation cellulaire, Facteurs temps, Humains, Immunité innée, Interféron bêta (immunologie), Interféron bêta (métabolisme), Interférons, Interleukines (immunologie), Interleukines (métabolisme), Libération de particules virales, Muqueuse respiratoire (cytologie), Muqueuse respiratoire (immunologie), Muqueuse respiratoire (virologie), Peptidyl-Dipeptidase A (immunologie), Peptidyl-Dipeptidase A (métabolisme), Récepteurs viraux (métabolisme), Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (immunologie).
- MESH :
- cytologie : Alvéoles pulmonaires, Muqueuse respiratoire.
- immunologie : Alvéoles pulmonaires, Antigènes viraux, Cellules épithéliales, Cytoplasme, Interféron bêta, Interleukines, Muqueuse respiratoire, Peptidyl-Dipeptidase A, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : ARN messager, Antigènes viraux, Interféron bêta, Interleukines, Peptidyl-Dipeptidase A, Récepteurs viraux.
- virologie : Alvéoles pulmonaires, Cellules épithéliales, Cytoplasme, Muqueuse respiratoire.
- ultrastructure : Culture primaire de cellules, Cytoplasme, Différenciation cellulaire, Facteurs temps, Humains, Immunité innée, Interférons, Libération de particules virales.
English descriptors
- KwdEn :
- Antigens, Viral (immunology), Antigens, Viral (metabolism), Cell Differentiation, Cytoplasm (immunology), Cytoplasm (ultrastructure), Cytoplasm (virology), Epithelial Cells (immunology), Epithelial Cells (virology), Humans, Immunity, Innate, Interferon-beta (immunology), Interferon-beta (metabolism), Interferons, Interleukins (immunology), Interleukins (metabolism), Peptidyl-Dipeptidase A (immunology), Peptidyl-Dipeptidase A (metabolism), Primary Cell Culture, Pulmonary Alveoli (cytology), Pulmonary Alveoli (immunology), Pulmonary Alveoli (virology), RNA, Messenger (metabolism), Receptors, Virus (metabolism), Respiratory Mucosa (cytology), Respiratory Mucosa (immunology), Respiratory Mucosa (virology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Time Factors, Virus Release.
- MESH :
- chemical , immunology : Antigens, Viral, Interferon-beta, Interleukins, Peptidyl-Dipeptidase A.
- chemical , metabolism : Antigens, Viral, Interferon-beta, Interleukins, Peptidyl-Dipeptidase A, RNA, Messenger, Receptors, Virus.
- cytology : Pulmonary Alveoli, Respiratory Mucosa.
- immunology : Cytoplasm, Epithelial Cells, Pulmonary Alveoli, Respiratory Mucosa, SARS Virus, Severe Acute Respiratory Syndrome.
- ultrastructure : Cytoplasm.
- virology : Cytoplasm, Epithelial Cells, Pulmonary Alveoli, Respiratory Mucosa.
- Cell Differentiation, Humans, Immunity, Innate, Interferons, Primary Cell Culture, Time Factors, Virus Release.
Abstract
Severe acute respiratory syndrome (SARS)-coronavirus (CoV) produces a devastating primary viral pneumonia with diffuse alveolar damage and a marked increase in circulating cytokines. One of the major cell types to be infected is the alveolar type II cell. However, the innate immune response of primary human alveolar epithelial cells infected with SARS-CoV has not been defined. Our objectives included developing a culture system permissive for SARS-CoV infection in primary human type II cells and defining their innate immune response. Culturing primary human alveolar type II cells at an air-liquid interface (A/L) improved their differentiation and greatly increased their susceptibility to infection, allowing us to define their primary interferon and chemokine responses. Viral antigens were detected in the cytoplasm of infected type II cells, electron micrographs demonstrated secretory vesicles filled with virions, virus RNA concentrations increased with time, and infectious virions were released by exocytosis from the apical surface of polarized type II cells. A marked increase was evident in the mRNA concentrations of interferon-β and interferon-λ (IL-29) and in a large number of proinflammatory cytokines and chemokines. A surprising finding involved the variability of expression of angiotensin-converting enzyme-2, the SARS-CoV receptor, in type II cells from different donors. In conclusion, the cultivation of alveolar type II cells at an air-liquid interface provides primary cultures in which to study the pulmonary innate immune responses to infection with SARS-CoV, and to explore possible therapeutic approaches to modulating these innate immune responses.
DOI: 10.1165/rcmb.2012-0339OC
PubMed: 23418343
Affiliations:
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Travanty</name></author><author><name sortKey="Oko, Lauren" sort="Oko, Lauren" uniqKey="Oko L" first="Lauren" last="Oko">Lauren Oko</name></author><author><name sortKey="Edeen, Karen" sort="Edeen, Karen" uniqKey="Edeen K" first="Karen" last="Edeen">Karen Edeen</name></author><author><name sortKey="Berglund, Andrew" sort="Berglund, Andrew" uniqKey="Berglund A" first="Andrew" last="Berglund">Andrew Berglund</name></author><author><name sortKey="Wang, Jieru" sort="Wang, Jieru" uniqKey="Wang J" first="Jieru" last="Wang">Jieru Wang</name></author><author><name sortKey="Ito, Yoko" sort="Ito, Yoko" uniqKey="Ito Y" first="Yoko" last="Ito">Yoko Ito</name></author><author><name sortKey="Holmes, Kathryn V" sort="Holmes, Kathryn V" uniqKey="Holmes K" first="Kathryn V" last="Holmes">Kathryn V. Holmes</name></author><author><name sortKey="Mason, Robert J" sort="Mason, Robert J" uniqKey="Mason R" first="Robert J" last="Mason">Robert J. Mason</name></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, Viral (immunology)</term><term>Antigens, Viral (metabolism)</term><term>Cell Differentiation</term><term>Cytoplasm (immunology)</term><term>Cytoplasm (ultrastructure)</term><term>Cytoplasm (virology)</term><term>Epithelial Cells (immunology)</term><term>Epithelial Cells (virology)</term><term>Humans</term><term>Immunity, Innate</term><term>Interferon-beta (immunology)</term><term>Interferon-beta (metabolism)</term><term>Interferons</term><term>Interleukins (immunology)</term><term>Interleukins (metabolism)</term><term>Peptidyl-Dipeptidase A (immunology)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Primary Cell Culture</term><term>Pulmonary Alveoli (cytology)</term><term>Pulmonary Alveoli (immunology)</term><term>Pulmonary Alveoli (virology)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, Virus (metabolism)</term><term>Respiratory Mucosa (cytology)</term><term>Respiratory Mucosa (immunology)</term><term>Respiratory Mucosa (virology)</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Time Factors</term><term>Virus Release</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Alvéoles pulmonaires (cytologie)</term><term>Alvéoles pulmonaires (immunologie)</term><term>Alvéoles pulmonaires (virologie)</term><term>Antigènes viraux (immunologie)</term><term>Antigènes viraux (métabolisme)</term><term>Cellules épithéliales (immunologie)</term><term>Cellules épithéliales (virologie)</term><term>Culture primaire de cellules</term><term>Cytoplasme (immunologie)</term><term>Cytoplasme (ultrastructure)</term><term>Cytoplasme (virologie)</term><term>Différenciation cellulaire</term><term>Facteurs temps</term><term>Humains</term><term>Immunité innée</term><term>Interféron bêta (immunologie)</term><term>Interféron bêta (métabolisme)</term><term>Interférons</term><term>Interleukines (immunologie)</term><term>Interleukines (métabolisme)</term><term>Libération de particules virales</term><term>Muqueuse respiratoire (cytologie)</term><term>Muqueuse respiratoire (immunologie)</term><term>Muqueuse respiratoire (virologie)</term><term>Peptidyl-Dipeptidase A (immunologie)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Récepteurs viraux (métabolisme)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Viral</term><term>Interferon-beta</term><term>Interleukins</term><term>Peptidyl-Dipeptidase 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xml:lang="en"><term>Cytoplasm</term><term>Epithelial Cells</term><term>Pulmonary Alveoli</term><term>Respiratory Mucosa</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Antigènes viraux</term><term>Interféron bêta</term><term>Interleukines</term><term>Peptidyl-Dipeptidase A</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Cytoplasm</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Alvéoles pulmonaires</term><term>Cellules épithéliales</term><term>Cytoplasme</term><term>Muqueuse respiratoire</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Cytoplasm</term><term>Epithelial Cells</term><term>Pulmonary Alveoli</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Differentiation</term><term>Humans</term><term>Immunity, Innate</term><term>Interferons</term><term>Primary Cell Culture</term><term>Time Factors</term><term>Virus Release</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="fr"><term>Culture primaire de cellules</term><term>Cytoplasme</term><term>Différenciation cellulaire</term><term>Facteurs temps</term><term>Humains</term><term>Immunité innée</term><term>Interférons</term><term>Libération de particules virales</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS)-coronavirus (CoV) produces a devastating primary viral pneumonia with diffuse alveolar damage and a marked increase in circulating cytokines. One of the major cell types to be infected is the alveolar type II cell. However, the innate immune response of primary human alveolar epithelial cells infected with SARS-CoV has not been defined. Our objectives included developing a culture system permissive for SARS-CoV infection in primary human type II cells and defining their innate immune response. Culturing primary human alveolar type II cells at an air-liquid interface (A/L) improved their differentiation and greatly increased their susceptibility to infection, allowing us to define their primary interferon and chemokine responses. Viral antigens were detected in the cytoplasm of infected type II cells, electron micrographs demonstrated secretory vesicles filled with virions, virus RNA concentrations increased with time, and infectious virions were released by exocytosis from the apical surface of polarized type II cells. A marked increase was evident in the mRNA concentrations of interferon-β and interferon-λ (IL-29) and in a large number of proinflammatory cytokines and chemokines. A surprising finding involved the variability of expression of angiotensin-converting enzyme-2, the SARS-CoV receptor, in type II cells from different donors. In conclusion, the cultivation of alveolar type II cells at an air-liquid interface provides primary cultures in which to study the pulmonary innate immune responses to infection with SARS-CoV, and to explore possible therapeutic approaches to modulating these innate immune responses.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><noCountry><name sortKey="Berglund, Andrew" sort="Berglund, Andrew" uniqKey="Berglund A" first="Andrew" last="Berglund">Andrew Berglund</name><name sortKey="Edeen, Karen" sort="Edeen, Karen" uniqKey="Edeen K" first="Karen" last="Edeen">Karen Edeen</name><name sortKey="Holmes, Kathryn V" sort="Holmes, Kathryn V" uniqKey="Holmes K" first="Kathryn V" last="Holmes">Kathryn V. Holmes</name><name sortKey="Ito, Yoko" sort="Ito, Yoko" uniqKey="Ito Y" first="Yoko" last="Ito">Yoko Ito</name><name sortKey="Mason, Robert J" sort="Mason, Robert J" uniqKey="Mason R" first="Robert J" last="Mason">Robert J. Mason</name><name sortKey="Oko, Lauren" sort="Oko, Lauren" uniqKey="Oko L" first="Lauren" last="Oko">Lauren Oko</name><name sortKey="Travanty, Emily A" sort="Travanty, Emily A" uniqKey="Travanty E" first="Emily A" last="Travanty">Emily A. Travanty</name><name sortKey="Wang, Jieru" sort="Wang, Jieru" uniqKey="Wang J" first="Jieru" last="Wang">Jieru Wang</name></noCountry><country name="États-Unis"><region name="Colorado"><name sortKey="Qian, Zhaohui" sort="Qian, Zhaohui" uniqKey="Qian Z" first="Zhaohui" last="Qian">Zhaohui Qian</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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