Nrf2 protects human alveolar epithelial cells against injury induced by influenza A virus.
Identifieur interne : 000569 ( PubMed/Corpus ); précédent : 000568; suivant : 000570Nrf2 protects human alveolar epithelial cells against injury induced by influenza A virus.
Auteurs : Beata Kosmider ; Elise M. Messier ; William J. Janssen ; Piruz Nahreini ; Jieru Wang ; Kevan L. Hartshorn ; Robert J. MasonSource :
- Respiratory research [ 1465-993X ] ; 2012.
English descriptors
- KwdEn :
- Adolescent, Cell Survival, Cells, Cultured, Child, Child, Preschool, Epithelial Cells (metabolism), Epithelial Cells (pathology), Epithelial Cells (virology), Female, Humans, Influenza A virus (physiology), Male, Pulmonary Alveoli (metabolism), Pulmonary Alveoli (pathology), Pulmonary Alveoli (virology).
- MESH :
- metabolism : Epithelial Cells, Pulmonary Alveoli.
- pathology : Epithelial Cells, Pulmonary Alveoli.
- physiology : Influenza A virus.
- virology : Epithelial Cells, Pulmonary Alveoli.
- Adolescent, Cell Survival, Cells, Cultured, Child, Child, Preschool, Female, Humans, Male.
Abstract
Influenza A virus (IAV) infection primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. Recent studies have shown the importance of lung antioxidant defense systems against injury by IAV. Nuclear factor-erythroid 2 related factor 2 (Nrf2) activates the majority of antioxidant genes.
DOI: 10.1186/1465-9921-13-43
PubMed: 22672594
Links to Exploration step
pubmed:22672594Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Nrf2 protects human alveolar epithelial cells against injury induced by influenza A virus.</title><author><name sortKey="Kosmider, Beata" sort="Kosmider, Beata" uniqKey="Kosmider B" first="Beata" last="Kosmider">Beata Kosmider</name><affiliation><nlm:affiliation>Department of Medicine, National Jewish Health, 1400 Jackson Street, Denver, CO 80206, USA. KosmiderB@NJHealth.org</nlm:affiliation></affiliation></author><author><name sortKey="Messier, Elise M" sort="Messier, Elise M" uniqKey="Messier E" first="Elise M" last="Messier">Elise M. Messier</name></author><author><name sortKey="Janssen, William J" sort="Janssen, William J" uniqKey="Janssen W" first="William J" last="Janssen">William J. Janssen</name></author><author><name sortKey="Nahreini, Piruz" sort="Nahreini, Piruz" uniqKey="Nahreini P" first="Piruz" last="Nahreini">Piruz Nahreini</name></author><author><name sortKey="Wang, Jieru" sort="Wang, Jieru" uniqKey="Wang J" first="Jieru" last="Wang">Jieru Wang</name></author><author><name sortKey="Hartshorn, Kevan L" sort="Hartshorn, Kevan L" uniqKey="Hartshorn K" first="Kevan L" last="Hartshorn">Kevan L. Hartshorn</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22672594</idno><idno type="pmid">22672594</idno><idno type="doi">10.1186/1465-9921-13-43</idno><idno type="wicri:Area/PubMed/Corpus">000569</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000569</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nrf2 protects human alveolar epithelial cells against injury induced by influenza A virus.</title><author><name sortKey="Kosmider, Beata" sort="Kosmider, Beata" uniqKey="Kosmider B" first="Beata" last="Kosmider">Beata Kosmider</name><affiliation><nlm:affiliation>Department of Medicine, National Jewish Health, 1400 Jackson Street, Denver, CO 80206, USA. KosmiderB@NJHealth.org</nlm:affiliation></affiliation></author><author><name sortKey="Messier, Elise M" sort="Messier, Elise M" uniqKey="Messier E" first="Elise M" last="Messier">Elise M. Messier</name></author><author><name sortKey="Janssen, William J" sort="Janssen, William J" uniqKey="Janssen W" first="William J" last="Janssen">William J. Janssen</name></author><author><name sortKey="Nahreini, Piruz" sort="Nahreini, Piruz" uniqKey="Nahreini P" first="Piruz" last="Nahreini">Piruz Nahreini</name></author><author><name sortKey="Wang, Jieru" sort="Wang, Jieru" uniqKey="Wang J" first="Jieru" last="Wang">Jieru Wang</name></author><author><name sortKey="Hartshorn, Kevan L" sort="Hartshorn, Kevan L" uniqKey="Hartshorn K" first="Kevan L" last="Hartshorn">Kevan L. Hartshorn</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">Respiratory research</title><idno type="eISSN">1465-993X</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Cell Survival</term><term>Cells, Cultured</term><term>Child</term><term>Child, Preschool</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (pathology)</term><term>Epithelial Cells (virology)</term><term>Female</term><term>Humans</term><term>Influenza A virus (physiology)</term><term>Male</term><term>Pulmonary Alveoli (metabolism)</term><term>Pulmonary Alveoli (pathology)</term><term>Pulmonary Alveoli (virology)</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Pulmonary Alveoli</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Epithelial Cells</term><term>Pulmonary Alveoli</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><term>Pulmonary Alveoli</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Cell Survival</term><term>Cells, Cultured</term><term>Child</term><term>Child, Preschool</term><term>Female</term><term>Humans</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza A virus (IAV) infection primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. Recent studies have shown the importance of lung antioxidant defense systems against injury by IAV. Nuclear factor-erythroid 2 related factor 2 (Nrf2) activates the majority of antioxidant genes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22672594</PMID><DateCompleted><Year>2013</Year><Month>05</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1465-993X</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><PubDate><Year>2012</Year><Month>Jun</Month><Day>06</Day></PubDate></JournalIssue><Title>Respiratory research</Title><ISOAbbreviation>Respir. Res.</ISOAbbreviation></Journal><ArticleTitle>Nrf2 protects human alveolar epithelial cells against injury induced by influenza A virus.</ArticleTitle><Pagination><MedlinePgn>43</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/1465-9921-13-43</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Influenza A virus (IAV) infection primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. Recent studies have shown the importance of lung antioxidant defense systems against injury by IAV. Nuclear factor-erythroid 2 related factor 2 (Nrf2) activates the majority of antioxidant genes.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Alveolar type II (ATII) cells and alveolar macrophages (AM) were isolated from human lungs not suitable for transplantation and donated for medical research. In some studies ATII cells were transdifferentiated to alveolar type I-like (ATI-like) cells. Alveolar epithelial cells were infected with A/PR/8/34 (PR8) virus. We analyzed PR8 virus production, influenza A nucleoprotein levels, ROS generation and expression of antiviral genes. Immunocytofluorescence was used to determine Nrf2 translocation and western blotting to detect Nrf2, HO-1 and caspase 1 and 3 cleavage. We also analyzed ingestion of PR8 virus infected apoptotic ATII cells by AM, cytokine levels by ELISA, glutathione levels, necrosis and apoptosis by TUNEL assay. Moreover, we determined the critical importance of Nrf2 using adenovirus Nrf2 (AdNrf2) or Nrf2 siRNA to overexpress or knockdown Nrf2, respectively.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We found that IAV induced oxidative stress, cytotoxicity and apoptosis in ATI-like and ATII cells. We also found that AM can ingest PR8 virus-induced apoptotic ATII cells (efferocytosis) but not viable cells, whereas ATII cells did not ingest these apoptotic cells. PR8 virus increased ROS production, Nrf2, HO-1, Mx1 and OAS1 expression and Nrf2 translocation to the nucleus. Nrf2 knockdown with siRNA sensitized ATI-like cells and ATII cells to injury induced by IAV and overexpression of Nrf2 with AdNrf2 protected these cells. Furthermore, Nrf2 overexpression followed by infection with PR8 virus decreased virus replication, influenza A nucleoprotein expression, antiviral response and oxidative stress. However, AdNrf2 did not increase IFN-λ1 (IL-29) levels.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our results indicate that IAV induces alveolar epithelial injury and that Nrf2 protects these cells from the cytopathic effects of IAV likely by increasing the expression of antioxidant genes. Identifying the pathways involved in protecting cells from injury during influenza infection may be particularly important for developing new therapeutic strategies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kosmider</LastName><ForeName>Beata</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Medicine, National Jewish Health, 1400 Jackson Street, Denver, CO 80206, USA. KosmiderB@NJHealth.org</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Messier</LastName><ForeName>Elise M</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Janssen</LastName><ForeName>William J</ForeName><Initials>WJ</Initials></Author><Author ValidYN="Y"><LastName>Nahreini</LastName><ForeName>Piruz</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jieru</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Hartshorn</LastName><ForeName>Kevan L</ForeName><Initials>KL</Initials></Author><Author ValidYN="Y"><LastName>Mason</LastName><ForeName>Robert J</ForeName><Initials>RJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL113655</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R03 AI101953</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5P01ESO18181</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5UO1AI082982</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>06</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Respir Res</MedlineTA><NlmUniqueID>101090633</NlmUniqueID><ISSNLinking>1465-9921</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" 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