Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection.
Identifieur interne : 000D49 ( Main/Exploration ); précédent : 000D48; suivant : 000D50Critical 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
Affiliations:
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52242.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Iowa</region></placeName><wicri:cityArea>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City</wicri:cityArea></affiliation></author><author><name sortKey="Hua, Xiaoyang" sort="Hua, Xiaoyang" uniqKey="Hua X" first="Xiaoyang" last="Hua">Xiaoyang Hua</name><affiliation wicri:level="2"><nlm:affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Iowa</region></placeName><wicri:cityArea>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City</wicri:cityArea></affiliation></author><author><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K" last="Meyerholz">David K. Meyerholz</name><affiliation wicri:level="2"><nlm:affiliation>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City, IA 52242.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Iowa</region></placeName><wicri:cityArea>Interdisciplinary Program in Immunology and Department of Otolaryngology, Department of Pathology, and Department of Microbiology, University of Iowa, Iowa City</wicri:cityArea></affiliation></author><author><name sortKey="Miki, Yoshimi" sort="Miki, Yoshimi" uniqKey="Miki Y" first="Yoshimi" last="Miki">Yoshimi Miki</name><affiliation wicri:level="1"><nlm:affiliation>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Yamamoto, Kei" sort="Yamamoto, Kei" uniqKey="Yamamoto K" first="Kei" last="Yamamoto">Kei Yamamoto</name><affiliation wicri:level="1"><nlm:affiliation>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Lipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Gelb, Michael" sort="Gelb, Michael" uniqKey="Gelb M" first="Michael" last="Gelb">Michael Gelb</name><affiliation wicri:level="2"><nlm: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.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Chemistry and Department of Biochemistry, University of Washington, Seattle, WA 98195 Department of Chemistry and Department of Biochemistry, University of Washington, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Murakami, Makoto" sort="Murakami, Makoto" uniqKey="Murakami M" first="Makoto" last="Murakami">Makoto Murakami</name><affiliation wicri:level="1"><nlm: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.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>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</wicri:regionArea><wicri:noRegion>Saitama 332-0012</wicri:noRegion></affiliation></author><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation wicri:level="4"><nlm: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.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>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</wicri:regionArea><orgName type="university">Université de l'Iowa</orgName><placeName><settlement type="city">Iowa City</settlement><region type="state">Iowa</region></placeName></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><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>Iowa</li><li>Région de Kantō</li><li>Washington (État)</li></region><settlement><li>Iowa City</li><li>Tokyo</li></settlement><orgName><li>Université de l'Iowa</li></orgName></list><tree><country name="États-Unis"><region name="Iowa"><name sortKey="Vijay, Rahul" sort="Vijay, Rahul" uniqKey="Vijay R" first="Rahul" last="Vijay">Rahul Vijay</name></region><name sortKey="Gelb, Michael" sort="Gelb, Michael" uniqKey="Gelb M" first="Michael" last="Gelb">Michael Gelb</name><name sortKey="Hua, Xiaoyang" sort="Hua, Xiaoyang" uniqKey="Hua X" first="Xiaoyang" last="Hua">Xiaoyang Hua</name><name sortKey="Meyerholz, David K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K" last="Meyerholz">David K. Meyerholz</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name></country><country name="Japon"><region name="Région de Kantō"><name sortKey="Miki, Yoshimi" sort="Miki, Yoshimi" uniqKey="Miki Y" first="Yoshimi" last="Miki">Yoshimi Miki</name></region><name sortKey="Murakami, Makoto" sort="Murakami, Makoto" uniqKey="Murakami M" first="Makoto" last="Murakami">Makoto Murakami</name><name sortKey="Yamamoto, Kei" sort="Yamamoto, Kei" uniqKey="Yamamoto K" first="Kei" last="Yamamoto">Kei Yamamoto</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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