Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells.
Identifieur interne : 000D30 ( Main/Exploration ); précédent : 000D29; suivant : 000D31Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells.
Auteurs : Nary Shin [Corée du Sud] ; Chul-Woong Pyo [Corée du Sud] ; Kwang Il Jung [Corée du Sud] ; Sang-Yun Choi [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2015.
Descripteurs français
- KwdFr :
- Alvéoles pulmonaires (cytologie), Alvéoles pulmonaires (enzymologie), Alvéoles pulmonaires (métabolisme), Animaux, Cellules rénales canines Madin-Darby, Chiens, Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire, Oxydoréduction, Protéines virales (physiologie), RT-PCR, Superoxide dismutase (métabolisme), Superoxide dismutase-1.
- MESH :
- cytologie : Alvéoles pulmonaires.
- enzymologie : Alvéoles pulmonaires.
- métabolisme : Alvéoles pulmonaires, Espèces réactives de l'oxygène, Superoxide dismutase.
- physiologie : Protéines virales.
- Animaux, Cellules rénales canines Madin-Darby, Chiens, Humains, Lignée cellulaire, Oxydoréduction, RT-PCR, Superoxide dismutase-1.
English descriptors
- KwdEn :
- Animals, Cell Line, Dogs, Humans, Madin Darby Canine Kidney Cells, Oxidation-Reduction, Pulmonary Alveoli (cytology), Pulmonary Alveoli (enzymology), Pulmonary Alveoli (metabolism), Reactive Oxygen Species (metabolism), Reverse Transcriptase Polymerase Chain Reaction, Superoxide Dismutase (metabolism), Superoxide Dismutase-1, Viral Proteins (physiology).
- MESH :
- chemical , metabolism : Reactive Oxygen Species, Superoxide Dismutase.
- cytology : Pulmonary Alveoli.
- enzymology : Pulmonary Alveoli.
- metabolism : Pulmonary Alveoli.
- chemical , physiology : Viral Proteins.
- Animals, Cell Line, Dogs, Humans, Madin Darby Canine Kidney Cells, Oxidation-Reduction, Reverse Transcriptase Polymerase Chain Reaction, Superoxide Dismutase-1.
Abstract
Occurrence of oxidative stress is common in influenza, and renders the host more susceptible to pathogenic effects including cell death. We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidative activity of PB1-F2 was directly reflected by cell viability and death. Infection with the mutant virus reduced the percentage of apoptotic cells more than two-fold compared to the wild-type IAV in A549 cells. Furthermore, expression of exogenous SOD1 gene abrogated a large portion of the PB1-F2-induced apoptosis of cells infected with wild-type IAV, but affected much less of the mutantΔF2 virus-infected cells. These results suggest that the PB1-F2 is directly implicated in virus-induced oxidative stress, thereby contributing to the early stages of IAV replication cycle and ultimately to disease severity.
DOI: 10.1016/j.bbrc.2015.03.010
PubMed: 25769947
Affiliations:
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Le document en format XML
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Electronic address: sychoi@korea.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Life Sciences, Korea University, Seoul 136-701</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Dogs</term><term>Humans</term><term>Madin Darby Canine Kidney Cells</term><term>Oxidation-Reduction</term><term>Pulmonary Alveoli (cytology)</term><term>Pulmonary Alveoli (enzymology)</term><term>Pulmonary Alveoli (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Superoxide Dismutase (metabolism)</term><term>Superoxide Dismutase-1</term><term>Viral Proteins (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alvéoles pulmonaires (cytologie)</term><term>Alvéoles pulmonaires (enzymologie)</term><term>Alvéoles pulmonaires (métabolisme)</term><term>Animaux</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lignée cellulaire</term><term>Oxydoréduction</term><term>Protéines virales (physiologie)</term><term>RT-PCR</term><term>Superoxide dismutase (métabolisme)</term><term>Superoxide dismutase-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Alvéoles pulmonaires</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Pulmonary Alveoli</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Alvéoles pulmonaires</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Pulmonary Alveoli</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Pulmonary Alveoli</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Alvéoles pulmonaires</term><term>Espèces réactives de l'oxygène</term><term>Superoxide dismutase</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Protéines virales</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Viral Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Dogs</term><term>Humans</term><term>Madin Darby Canine Kidney Cells</term><term>Oxidation-Reduction</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Superoxide Dismutase-1</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Humains</term><term>Lignée cellulaire</term><term>Oxydoréduction</term><term>RT-PCR</term><term>Superoxide dismutase-1</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Occurrence of oxidative stress is common in influenza, and renders the host more susceptible to pathogenic effects including cell death. We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidative activity of PB1-F2 was directly reflected by cell viability and death. Infection with the mutant virus reduced the percentage of apoptotic cells more than two-fold compared to the wild-type IAV in A549 cells. Furthermore, expression of exogenous SOD1 gene abrogated a large portion of the PB1-F2-induced apoptosis of cells infected with wild-type IAV, but affected much less of the mutantΔF2 virus-infected cells. These results suggest that the PB1-F2 is directly implicated in virus-induced oxidative stress, thereby contributing to the early stages of IAV replication cycle and ultimately to disease severity. </div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country><region><li>Région capitale de Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><region name="Région capitale de Séoul"><name sortKey="Shin, Nary" sort="Shin, Nary" uniqKey="Shin N" first="Nary" last="Shin">Nary Shin</name></region><name sortKey="Choi, Sang Yun" sort="Choi, Sang Yun" uniqKey="Choi S" first="Sang-Yun" last="Choi">Sang-Yun Choi</name><name sortKey="Jung, Kwang Il" sort="Jung, Kwang Il" uniqKey="Jung K" first="Kwang Il" last="Jung">Kwang Il Jung</name><name sortKey="Pyo, Chul Woong" sort="Pyo, Chul Woong" uniqKey="Pyo C" first="Chul-Woong" last="Pyo">Chul-Woong Pyo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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