Influenza A virus-induced autophagy contributes to enhancement of virus infectivity by SOD1 downregulation in alveolar epithelial cells.
Identifieur interne : 000995 ( Main/Exploration ); précédent : 000994; suivant : 000996Influenza A virus-induced autophagy contributes to enhancement of virus infectivity by SOD1 downregulation in alveolar epithelial cells.
Auteurs : Kwang Il Jung [Corée du Sud] ; Chul Woong Pyo [Corée du Sud] ; Sang-Yun Choi [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2018.
Descripteurs français
- KwdFr :
- Autophagie (physiologie), Cellules A549, Espèces réactives de l'oxygène, Extinction de l'expression des gènes, Grippe humaine (étiologie), Humains, Interactions hôte-pathogène, Pneumocytes (enzymologie), Pneumocytes (virologie), Protéines associées aux microtubules (génétique), Régulation négative, Superoxide dismutase-1 (métabolisme), Virus de la grippe A (pathogénicité).
- MESH :
- enzymologie : Pneumocytes.
- génétique : Protéines associées aux microtubules.
- métabolisme : Superoxide dismutase-1.
- pathogénicité : Virus de la grippe A.
- physiologie : Autophagie.
- virologie : Pneumocytes.
- étiologie : Grippe humaine.
- Cellules A549, Espèces réactives de l'oxygène, Extinction de l'expression des gènes, Humains, Interactions hôte-pathogène, Régulation négative.
English descriptors
- KwdEn :
- A549 Cells, Alveolar Epithelial Cells (enzymology), Alveolar Epithelial Cells (virology), Autophagy (physiology), Down-Regulation, Gene Silencing, Host-Pathogen Interactions, Humans, Influenza A virus (pathogenicity), Influenza, Human (etiology), Microtubule-Associated Proteins (genetics), Reactive Oxygen Species, Superoxide Dismutase-1 (metabolism).
- MESH :
- chemical , genetics : Microtubule-Associated Proteins.
- enzymology : Alveolar Epithelial Cells.
- etiology : Influenza, Human.
- chemical , metabolism : Superoxide Dismutase-1.
- pathogenicity : Influenza A virus.
- physiology : Autophagy.
- virology : Alveolar Epithelial Cells.
- A549 Cells, Down-Regulation, Gene Silencing, Host-Pathogen Interactions, Humans, Reactive Oxygen Species.
Abstract
Infection with influenza A virus (IAV) A/WSN/1933 (H1N1) causes oxidative stress and severe lung injury. We have demonstrated that the generation of reactive oxygen species (ROS) during IAV infection is tightly regulated by superoxide dismutase 1 (SOD1) and correlated with viral replication in alveolar epithelial cells. However, the molecular mechanism underlying SOD1 reduction during IAV infection is uncertain. Here we demonstrate that the autophagy pathway is activated by IAV infection and involved in enhanced ROS generation in the early phase of infection. We observed that IAV infection induced autophagic vacuolation, leading to autophagic degradation of cellular proteins, including the protease sensitive antioxidant SOD1. Silencing of the microtubule-associated protein 1A/1B-light chain 3 (LC3) gene in A549 cells supported the critical role of autophagy in the ROS increase. The decrease in viral titer and viral polymerase activity caused by LC3 silencing or the autophagy inhibitor clearly evidenced the involvement of autophagy in the control of ROS generation and viral infectivity. Therefore, we concluded that early stage IAV infection induces autophagic degradation of antioxidant enzyme SOD1, thereby contributing to increased ROS generation and viral infectivity in alveolar epithelial cells.
DOI: 10.1016/j.bbrc.2018.03.089
PubMed: 29548827
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="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Alveolar Epithelial Cells (enzymology)</term><term>Alveolar Epithelial Cells (virology)</term><term>Autophagy (physiology)</term><term>Down-Regulation</term><term>Gene Silencing</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Influenza A virus (pathogenicity)</term><term>Influenza, Human (etiology)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Reactive Oxygen Species</term><term>Superoxide Dismutase-1 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (physiologie)</term><term>Cellules A549</term><term>Espèces réactives de l'oxygène</term><term>Extinction de l'expression des gènes</term><term>Grippe humaine (étiologie)</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Pneumocytes (enzymologie)</term><term>Pneumocytes (virologie)</term><term>Protéines associées aux microtubules (génétique)</term><term>Régulation négative</term><term>Superoxide dismutase-1 (métabolisme)</term><term>Virus de la grippe A (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Pneumocytes</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Alveolar Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines associées aux microtubules</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Superoxide Dismutase-1</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Superoxide dismutase-1</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Pneumocytes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Alveolar Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Down-Regulation</term><term>Gene Silencing</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules A549</term><term>Espèces réactives de l'oxygène</term><term>Extinction de l'expression des gènes</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Régulation négative</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Infection with influenza A virus (IAV) A/WSN/1933 (H1N1) causes oxidative stress and severe lung injury. We have demonstrated that the generation of reactive oxygen species (ROS) during IAV infection is tightly regulated by superoxide dismutase 1 (SOD1) and correlated with viral replication in alveolar epithelial cells. However, the molecular mechanism underlying SOD1 reduction during IAV infection is uncertain. Here we demonstrate that the autophagy pathway is activated by IAV infection and involved in enhanced ROS generation in the early phase of infection. We observed that IAV infection induced autophagic vacuolation, leading to autophagic degradation of cellular proteins, including the protease sensitive antioxidant SOD1. Silencing of the microtubule-associated protein 1A/1B-light chain 3 (LC3) gene in A549 cells supported the critical role of autophagy in the ROS increase. The decrease in viral titer and viral polymerase activity caused by LC3 silencing or the autophagy inhibitor clearly evidenced the involvement of autophagy in the control of ROS generation and viral infectivity. Therefore, we concluded that early stage IAV infection induces autophagic degradation of antioxidant enzyme SOD1, thereby contributing to increased ROS generation and viral infectivity in alveolar epithelial cells.</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="Jung, Kwang Il" sort="Jung, Kwang Il" uniqKey="Jung K" first="Kwang Il" last="Jung">Kwang Il Jung</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="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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