Glutaredoxin-1 attenuates S-glutathionylation of the death receptor fas and decreases resolution of Pseudomonas aeruginosa pneumonia.
Identifieur interne : 000653 ( Main/Exploration ); précédent : 000652; suivant : 000654Glutaredoxin-1 attenuates S-glutathionylation of the death receptor fas and decreases resolution of Pseudomonas aeruginosa pneumonia.
Auteurs : Vikas Anathy ; Scott W. Aesif ; Sidra M. Hoffman ; Jenna L. Bement ; Amy S. Guala ; Karolyn G. Lahue ; Laurie W. Leclair ; Benjamin T. Suratt ; Carlyne D. Cool ; Matthew J. Wargo ; Yvonne M W. Janssen-HeiningerSource :
- American journal of respiratory and critical care medicine [ 1535-4970 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antigènes CD95 (métabolisme), Apoptose (MeSH), Bronchopneumonie (microbiologie), Bronchopneumonie (métabolisme), Caspases (métabolisme), Charge bactérienne (MeSH), Cytokines (métabolisme), Glutarédoxines (métabolisme), Glutathion (métabolisme), Humains (MeSH), Indice de gravité de la maladie (MeSH), Infections à Pseudomonas (microbiologie), Infections à Pseudomonas (métabolisme), Marqueurs biologiques (métabolisme), Muqueuse respiratoire (microbiologie), Muqueuse respiratoire (métabolisme), Mâle (MeSH), Oxydoréduction (MeSH), Poumon (microbiologie), Poumon (métabolisme), Pseudomonas aeruginosa (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH).
- MESH :
- microbiologie : Bronchopneumonie, Infections à Pseudomonas, Muqueuse respiratoire, Poumon.
- métabolisme : Antigènes CD95, Bronchopneumonie, Caspases, Cytokines, Glutarédoxines, Glutathion, Infections à Pseudomonas, Marqueurs biologiques, Muqueuse respiratoire, Poumon.
- Animaux, Apoptose, Charge bactérienne, Humains, Indice de gravité de la maladie, Mâle, Oxydoréduction, Pseudomonas aeruginosa, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (MeSH), Bacterial Load (MeSH), Biomarkers (metabolism), Bronchopneumonia (metabolism), Bronchopneumonia (microbiology), Caspases (metabolism), Cytokines (metabolism), Glutaredoxins (metabolism), Glutathione (metabolism), Humans (MeSH), Lung (metabolism), Lung (microbiology), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Oxidation-Reduction (MeSH), Pseudomonas Infections (metabolism), Pseudomonas Infections (microbiology), Pseudomonas aeruginosa (MeSH), Respiratory Mucosa (metabolism), Respiratory Mucosa (microbiology), Severity of Illness Index (MeSH), fas Receptor (metabolism).
- MESH :
- chemical , metabolism : Biomarkers, Caspases, Cytokines, Glutaredoxins, Glutathione, fas Receptor.
- metabolism : Bronchopneumonia, Lung, Pseudomonas Infections, Respiratory Mucosa.
- microbiology : Bronchopneumonia, Lung, Pseudomonas Infections, Respiratory Mucosa.
- Animals, Apoptosis, Bacterial Load, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxidation-Reduction, Pseudomonas aeruginosa, Severity of Illness Index.
Abstract
RATIONALE
The death receptor Fas is critical for bacterial clearance and survival of mice after Pseudomonas aeruginosa infection.
OBJECTIVES
Fas ligand (FasL)-induced apoptosis is augmented by S-glutathionylation of Fas (Fas-SSG), which can be reversed by glutaredoxin-1 (Grx1). Therefore, the objective of this study was to investigate the interplay between Grx1 and Fas in regulating the clearance of P. aeruginosa infection.
METHODS
Lung samples from patients with bronchopneumonia were analyzed by immunofluorescence. Primary tracheal epithelial cells, mice lacking the gene for Grx1 (Glrx1(-/-)), Glrx1(-/-) mice treated with caspase inhibitor, or transgenic mice overexpressing Grx1 in the airway epithelium were analyzed after infection with P. aeruginosa.
MEASUREMENTS AND MAIN RESULTS
Patient lung samples positive for P. aeruginosa infection demonstrated increased Fas-SSG compared with normal lung samples. Compared with wild-type primary lung epithelial cells, infection of Glrx1(-/-) cells with P. aeruginosa showed enhanced caspase 8 and 3 activities and cell death in association with increases in Fas-SSG. Infection of Glrx1(-/-) mice with P. aeruginosa resulted in enhanced caspase activity and increased Fas-SSG as compared with wild-type littermates. Absence of Glrx1 significantly enhanced bacterial clearance, and decreased mortality postinfection with P. aeruginosa. Inhibition of caspases significantly decreased bacterial clearance postinfection with P. aeruginosa, in association with decreased Fas-SSG. In contrast, transgenic mice that overexpress Grx1 in lung epithelial cells had significantly higher lung bacterial loads, enhanced mortality, decreased caspase activation, and Fas-SSG in the lung after infection with P. aeruginosa, compared with wild-type control animals.
CONCLUSIONS
These results suggest that S-glutathionylation of Fas within the lung epithelium enhances epithelial apoptosis and promotes clearance of P. aeruginosa and that glutaredoxin-1 impairs bacterial clearance and increases the severity of pneumonia in association with deglutathionylation of Fas.
DOI: 10.1164/rccm.201310-1905OC
PubMed: 24325366
PubMed Central: PMC3977722
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Aesif</name></author><author><name sortKey="Hoffman, Sidra M" sort="Hoffman, Sidra M" uniqKey="Hoffman S" first="Sidra M" last="Hoffman">Sidra M. Hoffman</name></author><author><name sortKey="Bement, Jenna L" sort="Bement, Jenna L" uniqKey="Bement J" first="Jenna L" last="Bement">Jenna L. Bement</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="Lahue, Karolyn G" sort="Lahue, Karolyn G" uniqKey="Lahue K" first="Karolyn G" last="Lahue">Karolyn G. Lahue</name></author><author><name sortKey="Leclair, Laurie W" sort="Leclair, Laurie W" uniqKey="Leclair L" first="Laurie W" last="Leclair">Laurie W. Leclair</name></author><author><name sortKey="Suratt, Benjamin T" sort="Suratt, Benjamin T" uniqKey="Suratt B" first="Benjamin T" last="Suratt">Benjamin T. Suratt</name></author><author><name sortKey="Cool, Carlyne D" sort="Cool, Carlyne D" uniqKey="Cool C" first="Carlyne D" last="Cool">Carlyne D. Cool</name></author><author><name sortKey="Wargo, Matthew J" sort="Wargo, Matthew J" uniqKey="Wargo M" first="Matthew J" last="Wargo">Matthew J. Wargo</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 and critical care medicine</title><idno type="eISSN">1535-4970</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Apoptosis (MeSH)</term><term>Bacterial Load (MeSH)</term><term>Biomarkers (metabolism)</term><term>Bronchopneumonia (metabolism)</term><term>Bronchopneumonia (microbiology)</term><term>Caspases (metabolism)</term><term>Cytokines (metabolism)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (metabolism)</term><term>Humans (MeSH)</term><term>Lung (metabolism)</term><term>Lung (microbiology)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Oxidation-Reduction (MeSH)</term><term>Pseudomonas Infections (metabolism)</term><term>Pseudomonas Infections (microbiology)</term><term>Pseudomonas aeruginosa (MeSH)</term><term>Respiratory Mucosa (metabolism)</term><term>Respiratory Mucosa (microbiology)</term><term>Severity of Illness Index (MeSH)</term><term>fas Receptor (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Antigènes CD95 (métabolisme)</term><term>Apoptose (MeSH)</term><term>Bronchopneumonie (microbiologie)</term><term>Bronchopneumonie (métabolisme)</term><term>Caspases (métabolisme)</term><term>Charge bactérienne (MeSH)</term><term>Cytokines (métabolisme)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Humains (MeSH)</term><term>Indice de gravité de la maladie (MeSH)</term><term>Infections à Pseudomonas (microbiologie)</term><term>Infections à Pseudomonas (métabolisme)</term><term>Marqueurs biologiques (métabolisme)</term><term>Muqueuse respiratoire (microbiologie)</term><term>Muqueuse respiratoire (métabolisme)</term><term>Mâle (MeSH)</term><term>Oxydoréduction (MeSH)</term><term>Poumon (microbiologie)</term><term>Poumon (métabolisme)</term><term>Pseudomonas aeruginosa (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>Caspases</term><term>Cytokines</term><term>Glutaredoxins</term><term>Glutathione</term><term>fas Receptor</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bronchopneumonia</term><term>Lung</term><term>Pseudomonas Infections</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Bronchopneumonie</term><term>Infections à Pseudomonas</term><term>Muqueuse respiratoire</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Bronchopneumonia</term><term>Lung</term><term>Pseudomonas Infections</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD95</term><term>Bronchopneumonie</term><term>Caspases</term><term>Cytokines</term><term>Glutarédoxines</term><term>Glutathion</term><term>Infections à Pseudomonas</term><term>Marqueurs biologiques</term><term>Muqueuse respiratoire</term><term>Poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Bacterial Load</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Oxidation-Reduction</term><term>Pseudomonas aeruginosa</term><term>Severity of Illness Index</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Charge bactérienne</term><term>Humains</term><term>Indice de gravité de la maladie</term><term>Mâle</term><term>Oxydoréduction</term><term>Pseudomonas aeruginosa</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>RATIONALE</b></p><p>The death receptor Fas is critical for bacterial clearance and survival of mice after Pseudomonas aeruginosa infection.</p></div><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b></p><p>Fas ligand (FasL)-induced apoptosis is augmented by S-glutathionylation of Fas (Fas-SSG), which can be reversed by glutaredoxin-1 (Grx1). Therefore, the objective of this study was to investigate the interplay between Grx1 and Fas in regulating the clearance of P. aeruginosa infection.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>Lung samples from patients with bronchopneumonia were analyzed by immunofluorescence. Primary tracheal epithelial cells, mice lacking the gene for Grx1 (Glrx1(-/-)), Glrx1(-/-) mice treated with caspase inhibitor, or transgenic mice overexpressing Grx1 in the airway epithelium were analyzed after infection with P. aeruginosa.</p></div><div type="abstract" xml:lang="en"><p><b>MEASUREMENTS AND MAIN RESULTS</b></p><p>Patient lung samples positive for P. aeruginosa infection demonstrated increased Fas-SSG compared with normal lung samples. Compared with wild-type primary lung epithelial cells, infection of Glrx1(-/-) cells with P. aeruginosa showed enhanced caspase 8 and 3 activities and cell death in association with increases in Fas-SSG. Infection of Glrx1(-/-) mice with P. aeruginosa resulted in enhanced caspase activity and increased Fas-SSG as compared with wild-type littermates. Absence of Glrx1 significantly enhanced bacterial clearance, and decreased mortality postinfection with P. aeruginosa. Inhibition of caspases significantly decreased bacterial clearance postinfection with P. aeruginosa, in association with decreased Fas-SSG. In contrast, transgenic mice that overexpress Grx1 in lung epithelial cells had significantly higher lung bacterial loads, enhanced mortality, decreased caspase activation, and Fas-SSG in the lung after infection with P. aeruginosa, compared with wild-type control animals.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>These results suggest that S-glutathionylation of Fas within the lung epithelium enhances epithelial apoptosis and promotes clearance of P. aeruginosa and that glutaredoxin-1 impairs bacterial clearance and increases the severity of pneumonia in association with deglutathionylation of Fas.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24325366</PMID><DateCompleted><Year>2014</Year><Month>04</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1535-4970</ISSN><JournalIssue CitedMedium="Internet"><Volume>189</Volume><Issue>4</Issue><PubDate><Year>2014</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>American journal of respiratory and critical care medicine</Title><ISOAbbreviation>Am J Respir Crit Care Med</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin-1 attenuates S-glutathionylation of the death receptor fas and decreases resolution of Pseudomonas aeruginosa pneumonia.</ArticleTitle><Pagination><MedlinePgn>463-74</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1164/rccm.201310-1905OC</ELocationID><Abstract><AbstractText Label="RATIONALE" NlmCategory="BACKGROUND">The death receptor Fas is critical for bacterial clearance and survival of mice after Pseudomonas aeruginosa infection.</AbstractText><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">Fas ligand (FasL)-induced apoptosis is augmented by S-glutathionylation of Fas (Fas-SSG), which can be reversed by glutaredoxin-1 (Grx1). Therefore, the objective of this study was to investigate the interplay between Grx1 and Fas in regulating the clearance of P. aeruginosa infection.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Lung samples from patients with bronchopneumonia were analyzed by immunofluorescence. Primary tracheal epithelial cells, mice lacking the gene for Grx1 (Glrx1(-/-)), Glrx1(-/-) mice treated with caspase inhibitor, or transgenic mice overexpressing Grx1 in the airway epithelium were analyzed after infection with P. aeruginosa.</AbstractText><AbstractText Label="MEASUREMENTS AND MAIN RESULTS" NlmCategory="RESULTS">Patient lung samples positive for P. aeruginosa infection demonstrated increased Fas-SSG compared with normal lung samples. Compared with wild-type primary lung epithelial cells, infection of Glrx1(-/-) cells with P. aeruginosa showed enhanced caspase 8 and 3 activities and cell death in association with increases in Fas-SSG. Infection of Glrx1(-/-) mice with P. aeruginosa resulted in enhanced caspase activity and increased Fas-SSG as compared with wild-type littermates. Absence of Glrx1 significantly enhanced bacterial clearance, and decreased mortality postinfection with P. aeruginosa. Inhibition of caspases significantly decreased bacterial clearance postinfection with P. aeruginosa, in association with decreased Fas-SSG. In contrast, transgenic mice that overexpress Grx1 in lung epithelial cells had significantly higher lung bacterial loads, enhanced mortality, decreased caspase activation, and Fas-SSG in the lung after infection with P. aeruginosa, compared with wild-type control animals.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These results suggest that S-glutathionylation of Fas within the lung epithelium enhances epithelial apoptosis and promotes clearance of P. aeruginosa and that glutaredoxin-1 impairs bacterial clearance and increases the severity of pneumonia in association with deglutathionylation of Fas.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Anathy</LastName><ForeName>Vikas</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>1 Department of Pathology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aesif</LastName><ForeName>Scott W</ForeName><Initials>SW</Initials></Author><Author ValidYN="Y"><LastName>Hoffman</LastName><ForeName>Sidra M</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Bement</LastName><ForeName>Jenna L</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Guala</LastName><ForeName>Amy S</ForeName><Initials>AS</Initials></Author><Author ValidYN="Y"><LastName>Lahue</LastName><ForeName>Karolyn G</ForeName><Initials>KG</Initials></Author><Author ValidYN="Y"><LastName>Leclair</LastName><ForeName>Laurie W</ForeName><Initials>LW</Initials></Author><Author ValidYN="Y"><LastName>Suratt</LastName><ForeName>Benjamin T</ForeName><Initials>BT</Initials></Author><Author ValidYN="Y"><LastName>Cool</LastName><ForeName>Carlyne D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Wargo</LastName><ForeName>Matthew J</ForeName><Initials>MJ</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>P20 RR021905</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI103003</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 ES007122</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL060014</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NCRR 1S10RR019246</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 RR019246</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL084200</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>R03 HL095404</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL079331</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 ES07122</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20 GM103496</GrantID><Acronym>GM</Acronym><Agency>NIGMS 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="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Respir Crit Care Med</MedlineTA><NlmUniqueID>9421642</NlmUniqueID><ISSNLinking>1073-449X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491901">FAS protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491899">Fas protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019014">fas Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D020169">Caspases</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Respir Crit Care Med. 2014 Feb 15;189(4):386-9</RefSource><PMID Version="1">24528316</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058491" MajorTopicYN="N">Bacterial Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" 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PubStatus="entrez"><Year>2013</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>4</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24325366</ArticleId><ArticleId IdType="doi">10.1164/rccm.201310-1905OC</ArticleId><ArticleId IdType="pmc">PMC3977722</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Science. 2000 Oct 20;290(5491):527-30</Citation><ArticleIdList><ArticleId IdType="pubmed">11039936</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 2002 Apr 1;165(7):867-903</Citation><ArticleIdList><ArticleId IdType="pubmed">11934711</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochemistry. 2001 Nov 27;40(47):14134-42</Citation><ArticleIdList><ArticleId IdType="pubmed">11714266</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2002 Mar;109(5):661-70</Citation><ArticleIdList><ArticleId IdType="pubmed">11877474</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2002 Apr;15(2):194-222</Citation><ArticleIdList><ArticleId IdType="pubmed">11932230</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2003 Aug;29(2):188-97</Citation><ArticleIdList><ArticleId IdType="pubmed">12878584</ArticleId></ArticleIdList></Reference><Reference><Citation>Hum Pathol. 2004 Aug;35(8):1000-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15297967</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol. 1994 Nov;267(5 Pt 1):L489-97</Citation><ArticleIdList><ArticleId IdType="pubmed">7977760</ArticleId></ArticleIdList></Reference><Reference><Citation>Thorax. 2005 Aug;60(8):659-64</Citation><ArticleIdList><ArticleId IdType="pubmed">16061707</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2006 Apr 15;176(8):4923-30</Citation><ArticleIdList><ArticleId IdType="pubmed">16585588</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Microbiol. 2006 Jul;8(7):1121-33</Citation><ArticleIdList><ArticleId IdType="pubmed">16819965</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2006 Aug 29;103(35):13086-91</Citation><ArticleIdList><ArticleId IdType="pubmed">16916935</ArticleId></ArticleIdList></Reference><Reference><Citation>Respir Res. 2006;7:133</Citation><ArticleIdList><ArticleId IdType="pubmed">17064412</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2007 Feb;36(2):147-51</Citation><ArticleIdList><ArticleId IdType="pubmed">16980552</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2007 Apr 27;282(17):12467-74</Citation><ArticleIdList><ArticleId IdType="pubmed">17324929</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiology. 2007 May;153(Pt 5):1329-38</Citation><ArticleIdList><ArticleId IdType="pubmed">17464047</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 2007 Nov 1;43(9):1299-312</Citation><ArticleIdList><ArticleId IdType="pubmed">17893043</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Sci. 2008 Apr 1;121(Pt 7):1036-45</Citation><ArticleIdList><ArticleId IdType="pubmed">18334556</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Exp Immunol. 2008 Sep;153(3):420-8</Citation><ArticleIdList><ArticleId IdType="pubmed">18647324</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Biol. 2009 Jan 26;184(2):241-52</Citation><ArticleIdList><ArticleId IdType="pubmed">19171757</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Pathol. 2009 Jul;175(1):36-45</Citation><ArticleIdList><ArticleId IdType="pubmed">19556513</ArticleId></ArticleIdList></Reference><Reference><Citation>Invest Ophthalmol Vis Sci. 2010 May;51(5):2537-47</Citation><ArticleIdList><ArticleId IdType="pubmed">20019368</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2010 Jul;78(7):2937-45</Citation><ArticleIdList><ArticleId IdType="pubmed">20457788</ArticleId></ArticleIdList></Reference><Reference><Citation>J Leukoc Biol. 2010 Nov;88(5):885-96</Citation><ArticleIdList><ArticleId IdType="pubmed">20566623</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 2011 Feb 1;183(3):356-63</Citation><ArticleIdList><ArticleId IdType="pubmed">20813889</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2011 Mar;121(3):1174-90</Citation><ArticleIdList><ArticleId IdType="pubmed">21285513</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Microbiol. 2012 Jan;14(1):95-106</Citation><ArticleIdList><ArticleId IdType="pubmed">21951860</ArticleId></ArticleIdList></Reference><Reference><Citation>Antioxid Redox Signal. 2012 Mar 15;16(6):496-505</Citation><ArticleIdList><ArticleId IdType="pubmed">21929356</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2012 Sep;32(17):3464-78</Citation><ArticleIdList><ArticleId IdType="pubmed">22751926</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2012 Sep 15;303(6):L528-38</Citation><ArticleIdList><ArticleId IdType="pubmed">22752969</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur Respir J. 2013 Feb;41(2):469-72</Citation><ArticleIdList><ArticleId IdType="pubmed">23370801</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2013 Sep;49(3):463-70</Citation><ArticleIdList><ArticleId 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Aesif</name><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name><name sortKey="Bement, Jenna L" sort="Bement, Jenna L" uniqKey="Bement J" first="Jenna L" last="Bement">Jenna L. Bement</name><name sortKey="Cool, Carlyne D" sort="Cool, Carlyne D" uniqKey="Cool C" first="Carlyne D" last="Cool">Carlyne D. Cool</name><name sortKey="Guala, Amy S" sort="Guala, Amy S" uniqKey="Guala A" first="Amy S" last="Guala">Amy S. Guala</name><name sortKey="Hoffman, Sidra M" sort="Hoffman, Sidra M" uniqKey="Hoffman S" first="Sidra M" last="Hoffman">Sidra M. Hoffman</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="Lahue, Karolyn G" sort="Lahue, Karolyn G" uniqKey="Lahue K" first="Karolyn G" last="Lahue">Karolyn G. Lahue</name><name sortKey="Leclair, Laurie W" sort="Leclair, Laurie W" uniqKey="Leclair L" first="Laurie W" last="Leclair">Laurie W. Leclair</name><name sortKey="Suratt, Benjamin T" sort="Suratt, Benjamin T" uniqKey="Suratt B" first="Benjamin T" last="Suratt">Benjamin T. Suratt</name><name sortKey="Wargo, Matthew J" sort="Wargo, Matthew J" uniqKey="Wargo M" first="Matthew J" last="Wargo">Matthew J. Wargo</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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