FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.
Identifieur interne : 000528 ( PubMed/Checkpoint ); précédent : 000527; suivant : 000529FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.
Auteurs : Fabienne Gally [États-Unis] ; Beata Kosmider ; Michael R. Weaver ; Kathryn M. Pate ; Kevan L. Hartshorn ; Rebecca E. Oberley-DeeganSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2013.
Descripteurs français
- KwdFr :
- ARN messager (génétique), Animaux, Cellules cultivées, Grippe humaine (), Grippe humaine (immunologie), Grippe humaine (virologie), Humains, Immunité acquise, Immunoprécipitation, Peroxydation lipidique, Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (métabolisme), Pneumopathie infectieuse (étiologie), Protéines de liaison aux acides gras (physiologie), Protéines tumorales (physiologie), RT-PCR, Réaction de polymérisation en chaine en temps réel, Récepteur PPAR gamma (métabolisme), Souris, Souris de lignée C57BL, Souris knockout, Sous-type H1N1 du virus de la grippe A (pathogénicité), Stress oxydatif, Susceptibilité à une maladie, Technique d'immunofluorescence, Technique de Western, Techniques immunoenzymatiques, Test ELISA.
- MESH :
- anatomopathologie : Pneumopathie infectieuse.
- génétique : ARN messager.
- immunologie : Grippe humaine.
- métabolisme : Pneumopathie infectieuse, Récepteur PPAR gamma.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- physiologie : Protéines de liaison aux acides gras, Protéines tumorales.
- virologie : Grippe humaine.
- étiologie : Pneumopathie infectieuse.
- Animaux, Cellules cultivées, Grippe humaine, Humains, Immunité acquise, Immunoprécipitation, Peroxydation lipidique, RT-PCR, Réaction de polymérisation en chaine en temps réel, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif, Susceptibilité à une maladie, Technique d'immunofluorescence, Technique de Western, Techniques immunoenzymatiques, Test ELISA.
English descriptors
- KwdEn :
- Adaptive Immunity, Animals, Blotting, Western, Cells, Cultured, Disease Susceptibility, Enzyme-Linked Immunosorbent Assay, Fatty Acid-Binding Proteins (physiology), Fluorescent Antibody Technique, Humans, Immunoenzyme Techniques, Immunoprecipitation, Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza, Human (complications), Influenza, Human (immunology), Influenza, Human (virology), Lipid Peroxidation, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasm Proteins (physiology), Oxidative Stress, PPAR gamma (metabolism), Pneumonia (etiology), Pneumonia (metabolism), Pneumonia (pathology), RNA, Messenger (genetics), Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction.
- MESH :
- chemical , genetics : RNA, Messenger.
- chemical , metabolism : PPAR gamma.
- chemical , physiology : Fatty Acid-Binding Proteins, Neoplasm Proteins.
- complications : Influenza, Human.
- etiology : Pneumonia.
- immunology : Influenza, Human.
- metabolism : Pneumonia.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- pathology : Pneumonia.
- virology : Influenza, Human.
- Adaptive Immunity, Animals, Blotting, Western, Cells, Cultured, Disease Susceptibility, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Humans, Immunoenzyme Techniques, Immunoprecipitation, Lipid Peroxidation, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxidative Stress, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
The early inflammatory response to influenza A virus infection contributes to severe lung disease and continues to pose a serious threat to human health. The mechanisms by which inflammatory cells invade the respiratory tract remain unclear. Uncontrolled inflammation and oxidative stress cause lung damage in response to influenza A infection. We have previously shown that the fatty acid binding protein 5 (FABP5) has anti-inflammatory properties. We speculate that, as a transporter of fatty acids, FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and wild-type (WT) mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils compared with WT mice. FABP5-/- mice presented lower viral burden but lost as much weight as WT mice. The adaptive immune response was also increased in FABP5-/- mice as illustrated by the accumulation of T and B cells in the lung tissues and increased levels of H1N1-specific IgG antibodies. FABP5 deficiency greatly enhanced oxidative damage and lipid peroxidation following influenza A infection and presented with sustained tissue inflammation. Interestingly, FABP5 expression decreased following influenza A infection in WT lung tissues that corresponded to a decrease in the anti-inflammatory molecule PPAR-γ activity. In conclusion, our results demonstrate a previously unknown contribution of FABP5 to influenza A virus pathogenesis by controlling excessive oxidative damage and inflammation. This property could be exploited for therapeutic purposes.
DOI: 10.1152/ajplung.00276.2012
PubMed: 23624787
Affiliations:
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Weaver</name></author><author><name sortKey="Pate, Kathryn M" sort="Pate, Kathryn M" uniqKey="Pate K" first="Kathryn M" last="Pate">Kathryn M. Pate</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="Oberley Deegan, Rebecca E" sort="Oberley Deegan, Rebecca E" uniqKey="Oberley Deegan R" first="Rebecca E" last="Oberley-Deegan">Rebecca E. 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Stress</term><term>Real-Time Polymerase Chain Reaction</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Grippe humaine</term><term>Humains</term><term>Immunité acquise</term><term>Immunoprécipitation</term><term>Peroxydation lipidique</term><term>RT-PCR</term><term>Réaction de polymérisation en chaine en temps réel</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Stress oxydatif</term><term>Susceptibilité à une maladie</term><term>Technique d'immunofluorescence</term><term>Technique de Western</term><term>Techniques immunoenzymatiques</term><term>Test ELISA</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The early inflammatory response to influenza A virus infection contributes to severe lung disease and continues to pose a serious threat to human health. The mechanisms by which inflammatory cells invade the respiratory tract remain unclear. Uncontrolled inflammation and oxidative stress cause lung damage in response to influenza A infection. We have previously shown that the fatty acid binding protein 5 (FABP5) has anti-inflammatory properties. We speculate that, as a transporter of fatty acids, FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and wild-type (WT) mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils compared with WT mice. FABP5-/- mice presented lower viral burden but lost as much weight as WT mice. The adaptive immune response was also increased in FABP5-/- mice as illustrated by the accumulation of T and B cells in the lung tissues and increased levels of H1N1-specific IgG antibodies. FABP5 deficiency greatly enhanced oxidative damage and lipid peroxidation following influenza A infection and presented with sustained tissue inflammation. Interestingly, FABP5 expression decreased following influenza A infection in WT lung tissues that corresponded to a decrease in the anti-inflammatory molecule PPAR-γ activity. In conclusion, our results demonstrate a previously unknown contribution of FABP5 to influenza A virus pathogenesis by controlling excessive oxidative damage and inflammation. This property could be exploited for therapeutic purposes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23624787</PMID><DateCompleted><Year>2013</Year><Month>09</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1504</ISSN><JournalIssue CitedMedium="Internet"><Volume>305</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Lung cellular and molecular physiology</Title><ISOAbbreviation>Am. J. Physiol. Lung Cell Mol. Physiol.</ISOAbbreviation></Journal><ArticleTitle>FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.</ArticleTitle><Pagination><MedlinePgn>L64-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajplung.00276.2012</ELocationID><Abstract><AbstractText>The early inflammatory response to influenza A virus infection contributes to severe lung disease and continues to pose a serious threat to human health. The mechanisms by which inflammatory cells invade the respiratory tract remain unclear. Uncontrolled inflammation and oxidative stress cause lung damage in response to influenza A infection. We have previously shown that the fatty acid binding protein 5 (FABP5) has anti-inflammatory properties. We speculate that, as a transporter of fatty acids, FABP5 plays an important protective role against oxidative damage to lipids during infection as well. Using FABP5-/- and wild-type (WT) mice infected with influenza A virus, we showed that FABP5-/- mice had increased cell infiltration of macrophages and neutrophils compared with WT mice. FABP5-/- mice presented lower viral burden but lost as much weight as WT mice. The adaptive immune response was also increased in FABP5-/- mice as illustrated by the accumulation of T and B cells in the lung tissues and increased levels of H1N1-specific IgG antibodies. FABP5 deficiency greatly enhanced oxidative damage and lipid peroxidation following influenza A infection and presented with sustained tissue inflammation. Interestingly, FABP5 expression decreased following influenza A infection in WT lung tissues that corresponded to a decrease in the anti-inflammatory molecule PPAR-γ activity. In conclusion, our results demonstrate a previously unknown contribution of FABP5 to influenza A virus pathogenesis by controlling excessive oxidative damage and inflammation. This property could be exploited for therapeutic purposes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gally</LastName><ForeName>Fabienne</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Medicine, National Jewish Health, Denver, CO 80206, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kosmider</LastName><ForeName>Beata</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Weaver</LastName><ForeName>Michael R</ForeName><Initials>MR</Initials></Author><Author ValidYN="Y"><LastName>Pate</LastName><ForeName>Kathryn M</ForeName><Initials>KM</Initials></Author><Author ValidYN="Y"><LastName>Hartshorn</LastName><ForeName>Kevan L</ForeName><Initials>KL</Initials></Author><Author ValidYN="Y"><LastName>Oberley-Deegan</LastName><ForeName>Rebecca E</ForeName><Initials>RE</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL069031</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Lung Cell Mol Physiol</MedlineTA><NlmUniqueID>100901229</NlmUniqueID><ISSNLinking>1040-0605</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C082667">Fabp5 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050556">Fatty Acid-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009363">Neoplasm Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047495">PPAR gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D056704" MajorTopicYN="N">Adaptive Immunity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004198" MajorTopicYN="N">Disease Susceptibility</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004797" MajorTopicYN="N">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050556" MajorTopicYN="N">Fatty Acid-Binding Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005455" MajorTopicYN="N">Fluorescent Antibody Technique</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007124" MajorTopicYN="N">Immunoenzyme Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047468" MajorTopicYN="N">Immunoprecipitation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015227" MajorTopicYN="N">Lipid Peroxidation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009363" MajorTopicYN="N">Neoplasm Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047495" MajorTopicYN="N">PPAR gamma</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011014" MajorTopicYN="N">Pneumonia</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060888" MajorTopicYN="N">Real-Time Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">FABP5</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">influenza A</Keyword><Keyword MajorTopicYN="N">lipid peroxidation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>9</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23624787</ArticleId><ArticleId IdType="pii">ajplung.00276.2012</ArticleId><ArticleId IdType="doi">10.1152/ajplung.00276.2012</ArticleId><ArticleId 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IdType="pubmed">10088602</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><noCountry><name sortKey="Hartshorn, Kevan L" sort="Hartshorn, Kevan L" uniqKey="Hartshorn K" first="Kevan L" last="Hartshorn">Kevan L. Hartshorn</name><name sortKey="Kosmider, Beata" sort="Kosmider, Beata" uniqKey="Kosmider B" first="Beata" last="Kosmider">Beata Kosmider</name><name sortKey="Oberley Deegan, Rebecca E" sort="Oberley Deegan, Rebecca E" uniqKey="Oberley Deegan R" first="Rebecca E" last="Oberley-Deegan">Rebecca E. Oberley-Deegan</name><name sortKey="Pate, Kathryn M" sort="Pate, Kathryn M" uniqKey="Pate K" first="Kathryn M" last="Pate">Kathryn M. Pate</name><name sortKey="Weaver, Michael R" sort="Weaver, Michael R" uniqKey="Weaver M" first="Michael R" last="Weaver">Michael R. Weaver</name></noCountry><country name="États-Unis"><region name="Colorado"><name sortKey="Gally, Fabienne" sort="Gally, Fabienne" uniqKey="Gally F" first="Fabienne" last="Gally">Fabienne Gally</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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