Temporal changes in glutaredoxin 1 and protein s-glutathionylation in allergic airway inflammation.
Identifieur interne : 000505 ( Main/Exploration ); précédent : 000504; suivant : 000506Temporal changes in glutaredoxin 1 and protein s-glutathionylation in allergic airway inflammation.
Auteurs : Kanako Maki [Japon] ; Katsura Nagai [Japon] ; Masaru Suzuki [Japon] ; Takashi Inomata [Japon] ; Takayuki Yoshida [Japon] ; Masaharu Nishimura [Japon]Source :
- PloS one [ 1932-6203 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Asthme (anatomopathologie), Asthme (métabolisme), Cytokines (métabolisme), Glutarédoxines (métabolisme), Glutathion (métabolisme), Humains (MeSH), Inflammation (anatomopathologie), Inflammation (métabolisme), Liquide de lavage bronchoalvéolaire (MeSH), Macrophages alvéolaires (anatomopathologie), Macrophages alvéolaires (effets des médicaments et des substances chimiques), Macrophages alvéolaires (métabolisme), Modèles animaux de maladie humaine (MeSH), Poumon (anatomopathologie), Poumon (métabolisme), Souris (MeSH), Stress oxydatif (MeSH).
- MESH :
- anatomopathologie : Asthme, Inflammation, Macrophages alvéolaires, Poumon.
- effets des médicaments et des substances chimiques : Macrophages alvéolaires.
- métabolisme : Asthme, Cytokines, Glutarédoxines, Glutathion, Inflammation, Macrophages alvéolaires, Poumon.
- Animaux, Humains, Liquide de lavage bronchoalvéolaire, Modèles animaux de maladie humaine, Souris, Stress oxydatif.
English descriptors
- KwdEn :
- Animals (MeSH), Asthma (metabolism), Asthma (pathology), Bronchoalveolar Lavage Fluid (MeSH), Cytokines (metabolism), Disease Models, Animal (MeSH), Glutaredoxins (metabolism), Glutathione (metabolism), Humans (MeSH), Inflammation (metabolism), Inflammation (pathology), Lung (metabolism), Lung (pathology), Macrophages, Alveolar (drug effects), Macrophages, Alveolar (metabolism), Macrophages, Alveolar (pathology), Mice (MeSH), Oxidative Stress (MeSH).
- MESH :
- chemical , metabolism : Cytokines, Glutaredoxins, Glutathione.
- drug effects : Macrophages, Alveolar.
- metabolism : Asthma, Inflammation, Lung, Macrophages, Alveolar.
- pathology : Asthma, Inflammation, Lung, Macrophages, Alveolar.
- Animals, Bronchoalveolar Lavage Fluid, Disease Models, Animal, Humans, Mice, Oxidative Stress.
Abstract
INTRODUCTION
Asthma is a chronic inflammatory disorder of the airways, involving oxidative stress. Upon oxidative stress, glutathione covalently binds to protein thiols to protect them against irreversible oxidation. This posttranslational modification, known as protein S-glutathionylation, can be reversed by glutaredoxin 1 (Glrx1) under physiological condition. Glrx1 is known to increase in the lung tissues of a murine model of allergic airway inflammation. However, the temporal relationship between levels of Glrx1, protein S-glutathionylation, and glutathione in the lungs with allergic airway inflammation is not clearly understood.
METHODS
BALB/c mice received 3 aerosol challenges with ovalbumin (OVA) following sensitization to OVA. They were sacrificed at 6, 24, 48, or 72 h, or 8 days (5 mice per group), and the levels of Glrx1, protein S-glutathionylation, glutathione, and 25 cytokines/chemokines were evaluated in bronchoalveolar lavage fluid (BALF) and/or lung tissue.
RESULTS
Levels of Glrx1 in BALF were significantly elevated in the OVA 6 h (final challenge) group compared to those in the control, with concurrent increases in protein S-glutathionylation levels in the lungs, as well as total glutathione (reduced and oxidized) and oxidized glutathione in BALF. Protein S-glutathionylation levels were attenuated at 24 h, with significant increases in Glrx1 levels in lung tissues at 48 and 72 h. Glrx1 in alveolar macrophages was induced after 6 h. Glrx1 levels concomitantly increased with Th2/NF-κB-related cytokines and chemokines in BALF.
CONCLUSIONS
The temporal relationships of Glrx1 with protein S-glutathionylation, glutathione, and cytokines/chemokines were observed as dynamic changes in lungs with allergic airway inflammation, suggesting that Glrx1 and protein-SSG redox status may play important roles in the development of allergic airway inflammation.
DOI: 10.1371/journal.pone.0122986
PubMed: 25874776
PubMed Central: PMC4395207
Affiliations:
Links toward previous steps (curation, corpus...)
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sortKey="Maki, Kanako" sort="Maki, Kanako" uniqKey="Maki K" first="Kanako" last="Maki">Kanako Maki</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Nagai, Katsura" sort="Nagai, Katsura" uniqKey="Nagai K" first="Katsura" last="Nagai">Katsura Nagai</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Suzuki, Masaru" sort="Suzuki, Masaru" uniqKey="Suzuki M" first="Masaru" last="Suzuki">Masaru Suzuki</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Inomata, Takashi" sort="Inomata, Takashi" uniqKey="Inomata T" first="Takashi" last="Inomata">Takashi Inomata</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Yoshida, Takayuki" sort="Yoshida, Takayuki" uniqKey="Yoshida T" first="Takayuki" last="Yoshida">Takayuki Yoshida</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Nishimura, Masaharu" sort="Nishimura, Masaharu" uniqKey="Nishimura M" first="Masaharu" last="Nishimura">Masaharu Nishimura</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Hokkaido University School of Medicine, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Asthma (metabolism)</term><term>Asthma (pathology)</term><term>Bronchoalveolar Lavage Fluid (MeSH)</term><term>Cytokines (metabolism)</term><term>Disease Models, Animal (MeSH)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (metabolism)</term><term>Humans (MeSH)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Macrophages, Alveolar (drug effects)</term><term>Macrophages, Alveolar (metabolism)</term><term>Macrophages, Alveolar (pathology)</term><term>Mice (MeSH)</term><term>Oxidative Stress (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Asthme (anatomopathologie)</term><term>Asthme (métabolisme)</term><term>Cytokines (métabolisme)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Humains (MeSH)</term><term>Inflammation (anatomopathologie)</term><term>Inflammation (métabolisme)</term><term>Liquide de lavage bronchoalvéolaire (MeSH)</term><term>Macrophages alvéolaires (anatomopathologie)</term><term>Macrophages alvéolaires (effets des médicaments et des substances chimiques)</term><term>Macrophages alvéolaires (métabolisme)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Souris (MeSH)</term><term>Stress oxydatif (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Glutaredoxins</term><term>Glutathione</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Asthme</term><term>Inflammation</term><term>Macrophages alvéolaires</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages, Alveolar</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Macrophages alvéolaires</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Asthma</term><term>Inflammation</term><term>Lung</term><term>Macrophages, Alveolar</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Asthme</term><term>Cytokines</term><term>Glutarédoxines</term><term>Glutathion</term><term>Inflammation</term><term>Macrophages alvéolaires</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Asthma</term><term>Inflammation</term><term>Lung</term><term>Macrophages, Alveolar</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Bronchoalveolar Lavage Fluid</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Liquide de lavage bronchoalvéolaire</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Stress oxydatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>INTRODUCTION</b></p><p>Asthma is a chronic inflammatory disorder of the airways, involving oxidative stress. Upon oxidative stress, glutathione covalently binds to protein thiols to protect them against irreversible oxidation. This posttranslational modification, known as protein S-glutathionylation, can be reversed by glutaredoxin 1 (Glrx1) under physiological condition. Glrx1 is known to increase in the lung tissues of a murine model of allergic airway inflammation. However, the temporal relationship between levels of Glrx1, protein S-glutathionylation, and glutathione in the lungs with allergic airway inflammation is not clearly understood.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>BALB/c mice received 3 aerosol challenges with ovalbumin (OVA) following sensitization to OVA. They were sacrificed at 6, 24, 48, or 72 h, or 8 days (5 mice per group), and the levels of Glrx1, protein S-glutathionylation, glutathione, and 25 cytokines/chemokines were evaluated in bronchoalveolar lavage fluid (BALF) and/or lung tissue.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Levels of Glrx1 in BALF were significantly elevated in the OVA 6 h (final challenge) group compared to those in the control, with concurrent increases in protein S-glutathionylation levels in the lungs, as well as total glutathione (reduced and oxidized) and oxidized glutathione in BALF. Protein S-glutathionylation levels were attenuated at 24 h, with significant increases in Glrx1 levels in lung tissues at 48 and 72 h. Glrx1 in alveolar macrophages was induced after 6 h. Glrx1 levels concomitantly increased with Th2/NF-κB-related cytokines and chemokines in BALF.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>The temporal relationships of Glrx1 with protein S-glutathionylation, glutathione, and cytokines/chemokines were observed as dynamic changes in lungs with allergic airway inflammation, suggesting that Glrx1 and protein-SSG redox status may play important roles in the development of allergic airway inflammation.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25874776</PMID><DateCompleted><Year>2016</Year><Month>01</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>4</Issue><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Temporal changes in glutaredoxin 1 and protein s-glutathionylation in allergic airway inflammation.</ArticleTitle><Pagination><MedlinePgn>e0122986</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0122986</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Asthma is a chronic inflammatory disorder of the airways, involving oxidative stress. Upon oxidative stress, glutathione covalently binds to protein thiols to protect them against irreversible oxidation. This posttranslational modification, known as protein S-glutathionylation, can be reversed by glutaredoxin 1 (Glrx1) under physiological condition. Glrx1 is known to increase in the lung tissues of a murine model of allergic airway inflammation. However, the temporal relationship between levels of Glrx1, protein S-glutathionylation, and glutathione in the lungs with allergic airway inflammation is not clearly understood.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">BALB/c mice received 3 aerosol challenges with ovalbumin (OVA) following sensitization to OVA. They were sacrificed at 6, 24, 48, or 72 h, or 8 days (5 mice per group), and the levels of Glrx1, protein S-glutathionylation, glutathione, and 25 cytokines/chemokines were evaluated in bronchoalveolar lavage fluid (BALF) and/or lung tissue.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Levels of Glrx1 in BALF were significantly elevated in the OVA 6 h (final challenge) group compared to those in the control, with concurrent increases in protein S-glutathionylation levels in the lungs, as well as total glutathione (reduced and oxidized) and oxidized glutathione in BALF. Protein S-glutathionylation levels were attenuated at 24 h, with significant increases in Glrx1 levels in lung tissues at 48 and 72 h. Glrx1 in alveolar macrophages was induced after 6 h. Glrx1 levels concomitantly increased with Th2/NF-κB-related cytokines and chemokines in BALF.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The temporal relationships of Glrx1 with protein S-glutathionylation, glutathione, and cytokines/chemokines were observed as dynamic changes in lungs with allergic airway inflammation, suggesting that Glrx1 and protein-SSG redox status may play important roles in the development of allergic airway inflammation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maki</LastName><ForeName>Kanako</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagai</LastName><ForeName>Katsura</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suzuki</LastName><ForeName>Masaru</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Inomata</LastName><ForeName>Takashi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yoshida</LastName><ForeName>Takayuki</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nishimura</LastName><ForeName>Masaharu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.</Affiliation></AffiliationInfo></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>2015</Year><Month>04</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001249" MajorTopicYN="N">Asthma</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016676" MajorTopicYN="N">Macrophages, Alveolar</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>07</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>02</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>4</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>4</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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uniqKey="Maki K" first="Kanako" last="Maki">Kanako Maki</name></noRegion><name sortKey="Inomata, Takashi" sort="Inomata, Takashi" uniqKey="Inomata T" first="Takashi" last="Inomata">Takashi Inomata</name><name sortKey="Nagai, Katsura" sort="Nagai, Katsura" uniqKey="Nagai K" first="Katsura" last="Nagai">Katsura Nagai</name><name sortKey="Nishimura, Masaharu" sort="Nishimura, Masaharu" uniqKey="Nishimura M" first="Masaharu" last="Nishimura">Masaharu Nishimura</name><name sortKey="Suzuki, Masaru" sort="Suzuki, Masaru" uniqKey="Suzuki M" first="Masaru" last="Suzuki">Masaru Suzuki</name><name sortKey="Yoshida, Takayuki" sort="Yoshida, Takayuki" uniqKey="Yoshida T" first="Takayuki" last="Yoshida">Takayuki Yoshida</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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