Influenza virus replication in lung epithelial cells depends on redox-sensitive pathways activated by NOX4-derived ROS.
Identifieur interne : 000456 ( PubMed/Corpus ); précédent : 000455; suivant : 000457Influenza virus replication in lung epithelial cells depends on redox-sensitive pathways activated by NOX4-derived ROS.
Auteurs : Donatella Amatore ; Rossella Sgarbanti ; Katia Aquilano ; Sara Baldelli ; Dolores Limongi ; Livia Civitelli ; Lucia Nencioni ; Enrico Garaci ; Maria Rosa Ciriolo ; Anna Teresa PalamaraSource :
- Cellular microbiology [ 1462-5822 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Cells, Cultured, Epithelial Cells (enzymology), Epithelial Cells (virology), Gene Expression, Host-Pathogen Interactions, Humans, Influenza A virus (physiology), Mice, NADPH Oxidase 4, NADPH Oxidases (metabolism), Oxidation-Reduction, Reactive Oxygen Species (metabolism), Up-Regulation, Virus Replication.
- MESH :
- chemical , metabolism : NADPH Oxidases, Reactive Oxygen Species.
- chemical : NADPH Oxidase 4.
- enzymology : Epithelial Cells.
- physiology : Influenza A virus.
- virology : Epithelial Cells.
- Animals, Cells, Cultured, Gene Expression, Host-Pathogen Interactions, Humans, Mice, Oxidation-Reduction, Up-Regulation, Virus Replication.
Abstract
An overproduction of reactive oxygen species (ROS) mediated by NADPH oxidase 2 (NOX2) has been related to airway inflammation typical of influenza infection. Virus-induced oxidative stress may also control viral replication, but the mechanisms underlying ROS production, as well as their role in activating intracellular pathways and specific steps of viral life cycle under redox control have to be fully elucidated. In this study, we demonstrate that influenza A virus infection of lung epithelial cells causes a significant ROS increase that depends mainly on NOX4, which is upregulated at both mRNA and protein levels, while the expression of NOX2, the primary source of ROS in inflammatory cells, is downregulated. Inhibition of NOX4 activity through chemical inhibitors or RNA silencing blocks the ROS increase, prevents MAPK phosphorylation, and inhibits viral ribonucleoprotein (vRNP) nuclear export and viral release. Overall these data, obtained in cell lines and primary culture, describe a so far unrecognized role for NOX4-derived ROS in activating redox-regulated intracellular pathways during influenza virus infection and highlight their relevance in controlling specific steps of viral replication in epithelial cells. Pharmacological modulation of NOX4-mediated ROS production may open the way for new therapeutic approaches to fighting influenza by targeting cell and not the virus.
DOI: 10.1111/cmi.12343
PubMed: 25154738
Links to Exploration step
pubmed:25154738Le document en format XML
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CEINGE Advanced Biotechnology, Naples, 80145, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Sgarbanti, Rossella" sort="Sgarbanti, Rossella" uniqKey="Sgarbanti R" first="Rossella" last="Sgarbanti">Rossella Sgarbanti</name></author><author><name sortKey="Aquilano, Katia" sort="Aquilano, Katia" uniqKey="Aquilano K" first="Katia" last="Aquilano">Katia Aquilano</name></author><author><name sortKey="Baldelli, Sara" sort="Baldelli, Sara" uniqKey="Baldelli S" first="Sara" last="Baldelli">Sara Baldelli</name></author><author><name sortKey="Limongi, Dolores" sort="Limongi, Dolores" uniqKey="Limongi D" first="Dolores" last="Limongi">Dolores Limongi</name></author><author><name sortKey="Civitelli, Livia" sort="Civitelli, Livia" uniqKey="Civitelli L" first="Livia" last="Civitelli">Livia Civitelli</name></author><author><name sortKey="Nencioni, Lucia" sort="Nencioni, Lucia" uniqKey="Nencioni L" first="Lucia" last="Nencioni">Lucia Nencioni</name></author><author><name sortKey="Garaci, Enrico" sort="Garaci, Enrico" uniqKey="Garaci E" first="Enrico" last="Garaci">Enrico Garaci</name></author><author><name sortKey="Ciriolo, Maria Rosa" sort="Ciriolo, Maria Rosa" uniqKey="Ciriolo M" first="Maria Rosa" last="Ciriolo">Maria Rosa Ciriolo</name></author><author><name sortKey="Palamara, Anna Teresa" sort="Palamara, Anna Teresa" uniqKey="Palamara A" first="Anna Teresa" last="Palamara">Anna Teresa Palamara</name></author></analytic><series><title level="j">Cellular microbiology</title><idno type="eISSN">1462-5822</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>Cells, Cultured</term><term>Epithelial Cells (enzymology)</term><term>Epithelial Cells (virology)</term><term>Gene Expression</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Influenza A virus (physiology)</term><term>Mice</term><term>NADPH Oxidase 4</term><term>NADPH Oxidases (metabolism)</term><term>Oxidation-Reduction</term><term>Reactive Oxygen Species (metabolism)</term><term>Up-Regulation</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NADPH Oxidases</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>NADPH Oxidase 4</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Gene Expression</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Mice</term><term>Oxidation-Reduction</term><term>Up-Regulation</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An overproduction of reactive oxygen species (ROS) mediated by NADPH oxidase 2 (NOX2) has been related to airway inflammation typical of influenza infection. Virus-induced oxidative stress may also control viral replication, but the mechanisms underlying ROS production, as well as their role in activating intracellular pathways and specific steps of viral life cycle under redox control have to be fully elucidated. In this study, we demonstrate that influenza A virus infection of lung epithelial cells causes a significant ROS increase that depends mainly on NOX4, which is upregulated at both mRNA and protein levels, while the expression of NOX2, the primary source of ROS in inflammatory cells, is downregulated. Inhibition of NOX4 activity through chemical inhibitors or RNA silencing blocks the ROS increase, prevents MAPK phosphorylation, and inhibits viral ribonucleoprotein (vRNP) nuclear export and viral release. Overall these data, obtained in cell lines and primary culture, describe a so far unrecognized role for NOX4-derived ROS in activating redox-regulated intracellular pathways during influenza virus infection and highlight their relevance in controlling specific steps of viral replication in epithelial cells. Pharmacological modulation of NOX4-mediated ROS production may open the way for new therapeutic approaches to fighting influenza by targeting cell and not the virus. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25154738</PMID><DateCompleted><Year>2015</Year><Month>08</Month><Day>06</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1462-5822</ISSN><JournalIssue CitedMedium="Internet"><Volume>17</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Cellular microbiology</Title><ISOAbbreviation>Cell. Microbiol.</ISOAbbreviation></Journal><ArticleTitle>Influenza virus replication in lung epithelial cells depends on redox-sensitive pathways activated by NOX4-derived ROS.</ArticleTitle><Pagination><MedlinePgn>131-45</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/cmi.12343</ELocationID><Abstract><AbstractText>An overproduction of reactive oxygen species (ROS) mediated by NADPH oxidase 2 (NOX2) has been related to airway inflammation typical of influenza infection. Virus-induced oxidative stress may also control viral replication, but the mechanisms underlying ROS production, as well as their role in activating intracellular pathways and specific steps of viral life cycle under redox control have to be fully elucidated. In this study, we demonstrate that influenza A virus infection of lung epithelial cells causes a significant ROS increase that depends mainly on NOX4, which is upregulated at both mRNA and protein levels, while the expression of NOX2, the primary source of ROS in inflammatory cells, is downregulated. Inhibition of NOX4 activity through chemical inhibitors or RNA silencing blocks the ROS increase, prevents MAPK phosphorylation, and inhibits viral ribonucleoprotein (vRNP) nuclear export and viral release. Overall these data, obtained in cell lines and primary culture, describe a so far unrecognized role for NOX4-derived ROS in activating redox-regulated intracellular pathways during influenza virus infection and highlight their relevance in controlling specific steps of viral replication in epithelial cells. Pharmacological modulation of NOX4-mediated ROS production may open the way for new therapeutic approaches to fighting influenza by targeting cell and not the virus. </AbstractText><CopyrightInformation>© 2014 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Amatore</LastName><ForeName>Donatella</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Public Health and Infectious Diseases, Pasteur Institute-Fondazione Cenci-Bolognetti, Sapienza University of Rome, Rome, 00185, Italy; CEINGE Advanced Biotechnology, Naples, 80145, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sgarbanti</LastName><ForeName>Rossella</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Aquilano</LastName><ForeName>Katia</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Baldelli</LastName><ForeName>Sara</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Limongi</LastName><ForeName>Dolores</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Civitelli</LastName><ForeName>Livia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Nencioni</LastName><ForeName>Lucia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Garaci</LastName><ForeName>Enrico</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Ciriolo</LastName><ForeName>Maria Rosa</ForeName><Initials>MR</Initials></Author><Author ValidYN="Y"><LastName>Palamara</LastName><ForeName>Anna Teresa</ForeName><Initials>AT</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>10</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell 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|étape= Corpus
|type= RBID
|clé= pubmed:25154738
|texte= Influenza virus replication in lung epithelial cells depends on redox-sensitive pathways activated by NOX4-derived ROS.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:25154738" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a StressCovidV1
| This area was generated with Dilib version V0.6.33. |  |