Ablation of glutaredoxin-1 attenuates lipopolysaccharide-induced lung inflammation and alveolar macrophage activation.
Identifieur interne : 000961 ( Main/Exploration ); précédent : 000960; suivant : 000962Ablation of glutaredoxin-1 attenuates lipopolysaccharide-induced lung inflammation and alveolar macrophage activation.
Auteurs : Scott W. Aesif [États-Unis] ; Vikas Anathy ; Ine Kuipers ; Amy S. Guala ; Jessica N. Reiss ; Ye-Shih Ho ; Yvonne M W. Janssen-HeiningerSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2011.
Descripteurs français
- KwdFr :
- Activation des macrophages (immunologie), Animaux (MeSH), Cytokines (métabolisme), Disulfures (métabolisme), Délétion de gène (MeSH), Facteur de transcription RelA (métabolisme), Forme de la cellule (MeSH), Glutarédoxines (déficit), Glutarédoxines (métabolisme), Glutathion (analogues et dérivés), Glutathion (métabolisme), Lipopolysaccharides (administration et posologie), Liquide de lavage bronchoalvéolaire (MeSH), Macrophages alvéolaires (anatomopathologie), Macrophages alvéolaires (immunologie), Noyau de la cellule (métabolisme), Numération cellulaire (MeSH), Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (métabolisme), Pneumopathie infectieuse (prévention et contrôle), Poumon (anatomopathologie), Poumon (métabolisme), Pénicillamine (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Transport des protéines (MeSH).
- MESH :
- administration et posologie : Lipopolysaccharides.
- analogues et dérivés : Glutathion.
- anatomopathologie : Macrophages alvéolaires, Pneumopathie infectieuse, Poumon.
- déficit : Glutarédoxines.
- immunologie : Activation des macrophages, Macrophages alvéolaires.
- métabolisme : Cytokines, Disulfures, Facteur de transcription RelA, Glutarédoxines, Glutathion, Noyau de la cellule, Pneumopathie infectieuse, Poumon, Pénicillamine.
- prévention et contrôle : Pneumopathie infectieuse.
- Animaux, Délétion de gène, Forme de la cellule, Liquide de lavage bronchoalvéolaire, Numération cellulaire, Souris, Souris de lignée C57BL, Transport des protéines.
English descriptors
- KwdEn :
- Animals (MeSH), Bronchoalveolar Lavage Fluid (MeSH), Cell Count (MeSH), Cell Nucleus (metabolism), Cell Shape (MeSH), Cytokines (metabolism), Disulfides (metabolism), Gene Deletion (MeSH), Glutaredoxins (deficiency), Glutaredoxins (metabolism), Glutathione (analogs & derivatives), Glutathione (metabolism), Lipopolysaccharides (administration & dosage), Lung (metabolism), Lung (pathology), Macrophage Activation (immunology), Macrophages, Alveolar (immunology), Macrophages, Alveolar (pathology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Penicillamine (metabolism), Pneumonia (metabolism), Pneumonia (pathology), Pneumonia (prevention & control), Protein Transport (MeSH), Transcription Factor RelA (metabolism).
- MESH :
- chemical , administration & dosage : Lipopolysaccharides.
- chemical , analogs & derivatives : Glutathione.
- chemical , deficiency : Glutaredoxins.
- chemical , metabolism : Cytokines, Disulfides, Glutaredoxins, Glutathione, Penicillamine, Transcription Factor RelA.
- immunology : Macrophage Activation, Macrophages, Alveolar.
- metabolism : Cell Nucleus, Lung, Pneumonia.
- pathology : Lung, Macrophages, Alveolar, Pneumonia.
- prevention & control : Pneumonia.
- Animals, Bronchoalveolar Lavage Fluid, Cell Count, Cell Shape, Gene Deletion, Mice, Mice, Inbred C57BL, Protein Transport.
Abstract
Protein S-glutathionylation (PSSG), a reversible posttranslational modification of reactive cysteines, recently emerged as a regulatory mechanism that affects diverse cell-signaling cascades. The extent of cellular PSSG is controlled by the oxidoreductase glutaredoxin-1 (Grx1), a cytosolic enzyme that specifically de-glutathionylates proteins. Here, we sought to evaluate the impact of the genetic ablation of Grx1 on PSSG and on LPS-induced lung inflammation. In response to LPS, Grx1 activity increased in lung tissue and bronchoalveolar lavage (BAL) fluid in WT (WT) mice compared with PBS control mice. Glrx1(-/-) mice consistently showed slight but statistically insignificant decreases in total numbers of inflammatory cells recovered by BAL. However, LPS-induced concentrations of IL-1β, TNF-α, IL-6, and Granulocyte/Monocyte Colony-Stimulating Factor (GM-CSF) in BAL were significantly decreased in Glrx1(-/-) mice compared with WT mice. An in situ assessment of PSSG reactivity and a biochemical evaluation of PSSG content demonstrated increases in the lung tissue of Glrx1(-/-) animals in response to LPS, compared with WT mice or PBS control mice. We also demonstrated that PSSG reactivity was prominent in alveolar macrophages (AMs). Comparative BAL analyses from WT and Glrx1(-/-) mice revealed fewer and smaller AMs in Glrx1(-/-) mice, which showed a significantly decreased expression of NF-κB family members, impaired nuclear translocation of RelA, and lower levels of NF-κB-dependent cytokines after exposure to LPS, compared with WT cells. Taken together, these results indicate that Grx1 regulates the production of inflammatory mediators through control of S-glutathionylation-sensitive signaling pathways such as NF-κB, and that Grx1 expression is critical to the activation of AMs.
DOI: 10.1165/rcmb.2009-0136OC
PubMed: 20539014
PubMed Central: PMC3095922
Affiliations:
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Aesif</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405</wicri:regionArea><placeName><region type="state">Vermont</region></placeName></affiliation></author><author><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name></author><author><name sortKey="Kuipers, Ine" sort="Kuipers, Ine" uniqKey="Kuipers I" first="Ine" last="Kuipers">Ine Kuipers</name></author><author><name sortKey="Guala, Amy S" sort="Guala, Amy S" uniqKey="Guala A" first="Amy S" last="Guala">Amy S. Guala</name></author><author><name sortKey="Reiss, Jessica N" sort="Reiss, Jessica N" uniqKey="Reiss J" first="Jessica N" last="Reiss">Jessica N. 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Aesif</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405</wicri:regionArea><placeName><region type="state">Vermont</region></placeName></affiliation></author><author><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name></author><author><name sortKey="Kuipers, Ine" sort="Kuipers, Ine" uniqKey="Kuipers I" first="Ine" last="Kuipers">Ine Kuipers</name></author><author><name sortKey="Guala, Amy S" sort="Guala, Amy S" uniqKey="Guala A" first="Amy S" last="Guala">Amy S. Guala</name></author><author><name sortKey="Reiss, Jessica N" sort="Reiss, Jessica N" uniqKey="Reiss J" first="Jessica N" last="Reiss">Jessica N. Reiss</name></author><author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name></author><author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Bronchoalveolar Lavage Fluid (MeSH)</term><term>Cell Count (MeSH)</term><term>Cell Nucleus (metabolism)</term><term>Cell Shape (MeSH)</term><term>Cytokines (metabolism)</term><term>Disulfides (metabolism)</term><term>Gene Deletion (MeSH)</term><term>Glutaredoxins (deficiency)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (analogs & derivatives)</term><term>Glutathione (metabolism)</term><term>Lipopolysaccharides (administration & dosage)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Macrophage Activation (immunology)</term><term>Macrophages, Alveolar (immunology)</term><term>Macrophages, Alveolar (pathology)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Penicillamine (metabolism)</term><term>Pneumonia (metabolism)</term><term>Pneumonia (pathology)</term><term>Pneumonia (prevention & control)</term><term>Protein Transport (MeSH)</term><term>Transcription Factor RelA (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des macrophages (immunologie)</term><term>Animaux (MeSH)</term><term>Cytokines (métabolisme)</term><term>Disulfures (métabolisme)</term><term>Délétion de gène (MeSH)</term><term>Facteur de transcription RelA (métabolisme)</term><term>Forme de la cellule (MeSH)</term><term>Glutarédoxines (déficit)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (analogues et dérivés)</term><term>Glutathion (métabolisme)</term><term>Lipopolysaccharides (administration et posologie)</term><term>Liquide de lavage bronchoalvéolaire (MeSH)</term><term>Macrophages alvéolaires (anatomopathologie)</term><term>Macrophages alvéolaires (immunologie)</term><term>Noyau de la cellule (métabolisme)</term><term>Numération cellulaire (MeSH)</term><term>Pneumopathie infectieuse (anatomopathologie)</term><term>Pneumopathie infectieuse (métabolisme)</term><term>Pneumopathie infectieuse (prévention et contrôle)</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Pénicillamine (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Transport des protéines (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Glutathione</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Disulfides</term><term>Glutaredoxins</term><term>Glutathione</term><term>Penicillamine</term><term>Transcription Factor RelA</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Glutathion</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Macrophages alvéolaires</term><term>Pneumopathie infectieuse</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation des macrophages</term><term>Macrophages alvéolaires</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophage Activation</term><term>Macrophages, Alveolar</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Nucleus</term><term>Lung</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Disulfures</term><term>Facteur de transcription RelA</term><term>Glutarédoxines</term><term>Glutathion</term><term>Noyau de la cellule</term><term>Pneumopathie infectieuse</term><term>Poumon</term><term>Pénicillamine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Macrophages, Alveolar</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Bronchoalveolar Lavage Fluid</term><term>Cell Count</term><term>Cell Shape</term><term>Gene Deletion</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Protein Transport</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Délétion de gène</term><term>Forme de la cellule</term><term>Liquide de lavage bronchoalvéolaire</term><term>Numération cellulaire</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Transport des protéines</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Protein S-glutathionylation (PSSG), a reversible posttranslational modification of reactive cysteines, recently emerged as a regulatory mechanism that affects diverse cell-signaling cascades. The extent of cellular PSSG is controlled by the oxidoreductase glutaredoxin-1 (Grx1), a cytosolic enzyme that specifically de-glutathionylates proteins. Here, we sought to evaluate the impact of the genetic ablation of Grx1 on PSSG and on LPS-induced lung inflammation. In response to LPS, Grx1 activity increased in lung tissue and bronchoalveolar lavage (BAL) fluid in WT (WT) mice compared with PBS control mice. Glrx1(-/-) mice consistently showed slight but statistically insignificant decreases in total numbers of inflammatory cells recovered by BAL. However, LPS-induced concentrations of IL-1β, TNF-α, IL-6, and Granulocyte/Monocyte Colony-Stimulating Factor (GM-CSF) in BAL were significantly decreased in Glrx1(-/-) mice compared with WT mice. An in situ assessment of PSSG reactivity and a biochemical evaluation of PSSG content demonstrated increases in the lung tissue of Glrx1(-/-) animals in response to LPS, compared with WT mice or PBS control mice. We also demonstrated that PSSG reactivity was prominent in alveolar macrophages (AMs). Comparative BAL analyses from WT and Glrx1(-/-) mice revealed fewer and smaller AMs in Glrx1(-/-) mice, which showed a significantly decreased expression of NF-κB family members, impaired nuclear translocation of RelA, and lower levels of NF-κB-dependent cytokines after exposure to LPS, compared with WT cells. Taken together, these results indicate that Grx1 regulates the production of inflammatory mediators through control of S-glutathionylation-sensitive signaling pathways such as NF-κB, and that Grx1 expression is critical to the activation of AMs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20539014</PMID><DateCompleted><Year>2011</Year><Month>06</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1535-4989</ISSN><JournalIssue CitedMedium="Internet"><Volume>44</Volume><Issue>4</Issue><PubDate><Year>2011</Year><Month>Apr</Month></PubDate></JournalIssue><Title>American journal of respiratory cell and molecular biology</Title><ISOAbbreviation>Am J Respir Cell Mol Biol</ISOAbbreviation></Journal><ArticleTitle>Ablation of glutaredoxin-1 attenuates lipopolysaccharide-induced lung inflammation and alveolar macrophage activation.</ArticleTitle><Pagination><MedlinePgn>491-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2009-0136OC</ELocationID><Abstract><AbstractText>Protein S-glutathionylation (PSSG), a reversible posttranslational modification of reactive cysteines, recently emerged as a regulatory mechanism that affects diverse cell-signaling cascades. The extent of cellular PSSG is controlled by the oxidoreductase glutaredoxin-1 (Grx1), a cytosolic enzyme that specifically de-glutathionylates proteins. Here, we sought to evaluate the impact of the genetic ablation of Grx1 on PSSG and on LPS-induced lung inflammation. In response to LPS, Grx1 activity increased in lung tissue and bronchoalveolar lavage (BAL) fluid in WT (WT) mice compared with PBS control mice. Glrx1(-/-) mice consistently showed slight but statistically insignificant decreases in total numbers of inflammatory cells recovered by BAL. However, LPS-induced concentrations of IL-1β, TNF-α, IL-6, and Granulocyte/Monocyte Colony-Stimulating Factor (GM-CSF) in BAL were significantly decreased in Glrx1(-/-) mice compared with WT mice. An in situ assessment of PSSG reactivity and a biochemical evaluation of PSSG content demonstrated increases in the lung tissue of Glrx1(-/-) animals in response to LPS, compared with WT mice or PBS control mice. We also demonstrated that PSSG reactivity was prominent in alveolar macrophages (AMs). Comparative BAL analyses from WT and Glrx1(-/-) mice revealed fewer and smaller AMs in Glrx1(-/-) mice, which showed a significantly decreased expression of NF-κB family members, impaired nuclear translocation of RelA, and lower levels of NF-κB-dependent cytokines after exposure to LPS, compared with WT cells. Taken together, these results indicate that Grx1 regulates the production of inflammatory mediators through control of S-glutathionylation-sensitive signaling pathways such as NF-κB, and that Grx1 expression is critical to the activation of AMs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aesif</LastName><ForeName>Scott W</ForeName><Initials>SW</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anathy</LastName><ForeName>Vikas</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Kuipers</LastName><ForeName>Ine</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Guala</LastName><ForeName>Amy S</ForeName><Initials>AS</Initials></Author><Author ValidYN="Y"><LastName>Reiss</LastName><ForeName>Jessica N</ForeName><Initials>JN</Initials></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Ye-Shih</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Janssen-Heininger</LastName><ForeName>Yvonne M W</ForeName><Initials>YM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL060014</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL079331</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL60014</GrantID><Acronym>HL</Acronym><Agency>NHLBI 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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>06</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Respir Cell Mol Biol</MedlineTA><NlmUniqueID>8917225</NlmUniqueID><ISSNLinking>1044-1549</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004220">Disulfides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051996">Transcription Factor RelA</NameOfSubstance></Chemical><Chemical><RegistryNumber>92000-26-5</RegistryNumber><NameOfSubstance UI="C061524">penicillamine-glutathione mixed disulfide</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>GNN1DV99GX</RegistryNumber><NameOfSubstance UI="D010396">Penicillamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002452" MajorTopicYN="N">Cell Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002467" MajorTopicYN="N">Cell Nucleus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048430" MajorTopicYN="N">Cell Shape</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004220" MajorTopicYN="N">Disulfides</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="Y">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</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="D008262" MajorTopicYN="N">Macrophage Activation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016676" MajorTopicYN="N">Macrophages, Alveolar</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred 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Guala</name><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name><name sortKey="Kuipers, Ine" sort="Kuipers, Ine" uniqKey="Kuipers I" first="Ine" last="Kuipers">Ine Kuipers</name><name sortKey="Reiss, Jessica N" sort="Reiss, Jessica N" uniqKey="Reiss J" first="Jessica N" last="Reiss">Jessica N. Reiss</name></noCountry><country name="États-Unis"><region name="Vermont"><name sortKey="Aesif, Scott W" sort="Aesif, Scott W" uniqKey="Aesif S" first="Scott W" last="Aesif">Scott W. Aesif</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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