Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection.
Identifieur interne : 000D62 ( PubMed/Curation ); précédent : 000D61; suivant : 000D63Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection.
Auteurs : Rahul Vijay [États-Unis] ; Xiaoyang Hua [États-Unis] ; David K. Meyerholz [États-Unis] ; Yoshimi Miki [Japon] ; Kei Yamamoto [Japon] ; Michael Gelb [États-Unis] ; Makoto Murakami [Japon] ; Stanley Perlman [États-Unis]Source :
- The Journal of experimental medicine [ 1540-9538 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- analyse : Lipides.
- immunologie : Poumon.
- physiologie : Cellules dendritiques, Group II Phospholipases A2.
- étiologie : Syndrome respiratoire aigu sévère.
- Animaux, Facteurs de l'âge, Humains, Immunité innée, Souris, Souris de lignée C57BL, Stress oxydatif, Susceptibilité à une maladie.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : CD11c Antigen, Lipids.
- etiology : Severe Acute Respiratory Syndrome.
- immunology : Lung.
- physiology : Dendritic Cells, Group II Phospholipases A2.
- Age Factors, Animals, Disease Susceptibility, Humans, Immunity, Innate, Mice, Mice, Inbred C57BL, Oxidative Stress.
Abstract
Oxidative stress and chronic low-grade inflammation in the lungs are associated with aging and may contribute to age-related immune dysfunction. To maintain lung homeostasis, chronic inflammation is countered by enhanced expression of proresolving/antiinflammatory factors. Here, we show that age-dependent increases of one such factor in the lungs, a phospholipase A2 (PLA2) group IID (PLA2G2D) with antiinflammatory properties, contributed to worse outcomes in mice infected with severe acute respiratory syndrome-coronavirus (SARS-CoV). Strikingly, infection of mice lacking PLA2G2D expression (Pla2g2d(-/-) mice) converted a uniformly lethal infection to a nonlethal one (>80% survival), subsequent to development of enhanced respiratory DC migration to the draining lymph nodes, augmented antivirus T cell responses, and diminished lung damage. We also observed similar effects in influenza A virus-infected middle-aged Pla2g2d(-/-) mice. Furthermore, oxidative stress, probably via lipid peroxidation, was found to induce PLA2G2D expression in mice and in human monocyte-derived macrophages. Thus, our results suggest that directed inhibition of a single inducible phospholipase, PLA2G2D, in the lungs of older patients with severe respiratory infections is potentially an attractive therapeutic intervention to restore immune function.
DOI: 10.1084/jem.20150632
PubMed: 26392224
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Iowa, Iowa City</wicri:regionArea></affiliation></author></analytic><series><title level="j">The Journal of experimental medicine</title><idno type="eISSN">1540-9538</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>CD11c Antigen (analysis)</term><term>Dendritic Cells (physiology)</term><term>Disease Susceptibility</term><term>Group II Phospholipases A2 (physiology)</term><term>Humans</term><term>Immunity, Innate</term><term>Lipids (analysis)</term><term>Lung (immunology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Oxidative Stress</term><term>Severe Acute Respiratory Syndrome (etiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules dendritiques (physiologie)</term><term>Facteurs de l'âge</term><term>Group II Phospholipases A2 (physiologie)</term><term>Humains</term><term>Immunité innée</term><term>Lipides (analyse)</term><term>Poumon (immunologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif</term><term>Susceptibilité à une maladie</term><term>Syndrome respiratoire aigu sévère (étiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>CD11c Antigen</term><term>Lipids</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Lipides</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules dendritiques</term><term>Group II Phospholipases A2</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dendritic Cells</term><term>Group II Phospholipases A2</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Disease Susceptibility</term><term>Humans</term><term>Immunity, Innate</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Facteurs de l'âge</term><term>Humains</term><term>Immunité innée</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif</term><term>Susceptibilité à une maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress and chronic low-grade inflammation in the lungs are associated with aging and may contribute to age-related immune dysfunction. To maintain lung homeostasis, chronic inflammation is countered by enhanced expression of proresolving/antiinflammatory factors. Here, we show that age-dependent increases of one such factor in the lungs, a phospholipase A2 (PLA2) group IID (PLA2G2D) with antiinflammatory properties, contributed to worse outcomes in mice infected with severe acute respiratory syndrome-coronavirus (SARS-CoV). Strikingly, infection of mice lacking PLA2G2D expression (Pla2g2d(-/-) mice) converted a uniformly lethal infection to a nonlethal one (>80% survival), subsequent to development of enhanced respiratory DC migration to the draining lymph nodes, augmented antivirus T cell responses, and diminished lung damage. We also observed similar effects in influenza A virus-infected middle-aged Pla2g2d(-/-) mice. Furthermore, oxidative stress, probably via lipid peroxidation, was found to induce PLA2G2D expression in mice and in human monocyte-derived macrophages. Thus, our results suggest that directed inhibition of a single inducible phospholipase, PLA2G2D, in the lungs of older patients with severe respiratory infections is potentially an attractive therapeutic intervention to restore immune function. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26392224</PMID><DateCompleted><Year>2016</Year><Month>02</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1540-9538</ISSN><JournalIssue CitedMedium="Internet"><Volume>212</Volume><Issue>11</Issue><PubDate><Year>2015</Year><Month>Oct</Month><Day>19</Day></PubDate></JournalIssue><Title>The Journal of experimental medicine</Title><ISOAbbreviation>J. Exp. Med.</ISOAbbreviation></Journal><ArticleTitle>Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection.</ArticleTitle><Pagination><MedlinePgn>1851-68</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1084/jem.20150632</ELocationID><Abstract><AbstractText>Oxidative stress and chronic low-grade inflammation in the lungs are associated with aging and may contribute to age-related immune dysfunction. To maintain lung homeostasis, chronic inflammation is countered by enhanced expression of proresolving/antiinflammatory factors. Here, we show that age-dependent increases of one such factor in the lungs, a phospholipase A2 (PLA2) group IID (PLA2G2D) with antiinflammatory properties, contributed to worse outcomes in mice infected with severe acute respiratory syndrome-coronavirus (SARS-CoV). Strikingly, infection of mice lacking PLA2G2D expression (Pla2g2d(-/-) mice) converted a uniformly lethal infection to a nonlethal one (>80% survival), subsequent to development of enhanced respiratory DC migration to the draining lymph nodes, augmented antivirus T cell responses, and diminished lung damage. We also observed similar effects in influenza A virus-infected middle-aged Pla2g2d(-/-) mice. Furthermore, oxidative stress, probably via lipid peroxidation, was found to induce PLA2G2D expression in mice and in human monocyte-derived macrophages. Thus, our results suggest that directed inhibition of a single inducible phospholipase, PLA2G2D, in the lungs of older patients with severe respiratory infections is potentially an attractive therapeutic intervention to restore immune function. </AbstractText><CopyrightInformation>© 2015 Vijay et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vijay</LastName><ForeName>Rahul</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hua</LastName><ForeName>Xiaoyang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyerholz</LastName><ForeName>David K</ForeName><Initials>DK</Initials><AffiliationInfo><Affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miki</LastName><ForeName>Yoshimi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamamoto</LastName><ForeName>Kei</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gelb</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Chemistry and Department of Biochemistry, University of Washington, Seattle, WA 98195 Department of Chemistry and Department of Biochemistry, University of Washington, Seattle, WA 98195.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murakami</LastName><ForeName>Makoto</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perlman</LastName><ForeName>Stanley</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242 Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242 Stanley-Perlman@uiowa.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R37 HL036235</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI091322</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI091322</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI060699</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AI060699</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL036235</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK054759</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL36235</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><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>09</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Exp Med</MedlineTA><NlmUniqueID>2985109R</NlmUniqueID><ISSNLinking>0022-1007</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039521">CD11c Antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008055">Lipids</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.4</RegistryNumber><NameOfSubstance UI="D054501">Group II Phospholipases A2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Exp Med. 2015 Oct 19;212(11):1755</RefSource><PMID Version="1">26482140</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000367" MajorTopicYN="N">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D039521" 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