Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.
Identifieur interne : 000E96 ( Main/Merge ); précédent : 000E95; suivant : 000E97Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.
Auteurs : John C. Kash [États-Unis] ; Yongli Xiao [États-Unis] ; A Sally Davis [États-Unis] ; Kathie-Anne Walters [États-Unis] ; Daniel S. Chertow [États-Unis] ; Judith D. Easterbrook [États-Unis] ; Rebecca L. Dunfee [États-Unis] ; Aline Sandouk [États-Unis] ; Brett W. Jagger [États-Unis] ; Louis M. Schwartzman [États-Unis] ; Rolf E. Kuestner [États-Unis] ; Nancy B. Wehr [États-Unis] ; Karl Huffman [États-Unis] ; Rosalind A. Rosenthal [États-Unis] ; Adrian Ozinsky [États-Unis] ; Rodney L. Levine [États-Unis] ; Susan R. Doctrow [États-Unis] ; Jeffery K. Taubenberger [États-Unis]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2014.
Descripteurs français
- KwdFr :
- Analyse de survie, Animaux, Caspase-3 (génétique), Caspase-3 (métabolisme), Cellules rénales canines Madin-Darby, Charge virale, Chiens, Composés organométalliques (pharmacologie), Désoxyguanosine (analogues et dérivés), Désoxyguanosine (métabolisme), Espèces réactives de l'oxygène (antagonistes et inhibiteurs), Espèces réactives de l'oxygène (métabolisme), Expression des gènes, Femelle, Humains, Infections à Orthomyxoviridae (mortalité), Infections à Orthomyxoviridae (métabolisme), Infections à Orthomyxoviridae (traitement médicamenteux), Infections à Orthomyxoviridae (virologie), Inflammation (mortalité), Inflammation (métabolisme), Inflammation (traitement médicamenteux), Inflammation (virologie), Marqueurs biologiques (métabolisme), Pandémie de grippe de 1918-1919, Piégeurs de radicaux libres (pharmacologie), Poumon (), Poumon (anatomopathologie), Poumon (métabolisme), Réparation de l'ADN, Réplication virale, Souris, Souris de lignée BALB C, Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H1N1 du virus de la grippe A (physiologie).
- MESH :
- analogues et dérivés : Désoxyguanosine.
- anatomopathologie : Poumon.
- antagonistes et inhibiteurs : Espèces réactives de l'oxygène.
- génétique : Caspase-3.
- mortalité : Infections à Orthomyxoviridae, Inflammation.
- métabolisme : Caspase-3, Désoxyguanosine, Espèces réactives de l'oxygène, Infections à Orthomyxoviridae, Inflammation, Marqueurs biologiques, Poumon.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- pharmacologie : Composés organométalliques, Piégeurs de radicaux libres.
- physiologie : Sous-type H1N1 du virus de la grippe A.
- traitement médicamenteux : Infections à Orthomyxoviridae, Inflammation.
- virologie : Infections à Orthomyxoviridae, Inflammation.
- Analyse de survie, Animaux, Cellules rénales canines Madin-Darby, Charge virale, Chiens, Expression des gènes, Femelle, Humains, Pandémie de grippe de 1918-1919, Poumon, Réparation de l'ADN, Réplication virale, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- 8-Hydroxy-2'-Deoxyguanosine, Animals, Biomarkers (metabolism), Caspase 3 (genetics), Caspase 3 (metabolism), DNA Repair, Deoxyguanosine (analogs & derivatives), Deoxyguanosine (metabolism), Dogs, Female, Free Radical Scavengers (pharmacology), Gene Expression, Humans, Inflammation (drug therapy), Inflammation (metabolism), Inflammation (mortality), Inflammation (virology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H1N1 Subtype (physiology), Influenza Pandemic, 1918-1919, Lung (drug effects), Lung (metabolism), Lung (pathology), Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Organometallic Compounds (pharmacology), Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (metabolism), Orthomyxoviridae Infections (mortality), Orthomyxoviridae Infections (virology), Reactive Oxygen Species (antagonists & inhibitors), Reactive Oxygen Species (metabolism), Survival Analysis, Viral Load, Virus Replication.
- MESH :
- chemical , analogs & derivatives : Deoxyguanosine.
- chemical , antagonists & inhibitors : Reactive Oxygen Species.
- chemical , genetics : Caspase 3.
- chemical , metabolism : Biomarkers, Caspase 3, Deoxyguanosine, Reactive Oxygen Species.
- chemical , pharmacology : Free Radical Scavengers, Organometallic Compounds.
- chemical : 8-Hydroxy-2'-Deoxyguanosine.
- drug effects : Lung.
- drug therapy : Inflammation, Orthomyxoviridae Infections.
- metabolism : Inflammation, Lung, Orthomyxoviridae Infections.
- mortality : Inflammation, Orthomyxoviridae Infections.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- pathology : Lung.
- physiology : Influenza A Virus, H1N1 Subtype.
- virology : Inflammation, Orthomyxoviridae Infections.
- Animals, DNA Repair, Dogs, Female, Gene Expression, Humans, Influenza Pandemic, 1918-1919, Madin Darby Canine Kidney Cells, Mice, Mice, Inbred BALB C, Survival Analysis, Viral Load, Virus Replication.
Abstract
The 1918 influenza pandemic caused over 40 million deaths worldwide, with 675,000 deaths in the United States alone. Studies in several experimental animal models showed that 1918 influenza virus infection resulted in severe lung pathology associated with dysregulated immune and cell death responses. To determine if reactive oxygen species produced by host inflammatory responses play a central role in promoting severity of lung pathology, we treated 1918 influenza virus-infected mice with the catalytic catalase/superoxide dismutase mimetic, salen-manganese complex EUK-207 beginning 3 days postinfection. Postexposure treatment of mice infected with a lethal dose of the 1918 influenza virus with EUK-207 resulted in significantly increased survival and reduced lung pathology without a reduction in viral titers. In vitro studies also showed that EUK-207 treatment did not affect 1918 influenza viral replication. Immunohistochemical analysis showed a reduction in the detection of the apoptosis marker cleaved caspase-3 and the oxidative stress marker 8-oxo-2'-deoxyguanosine in lungs of EUK-207-treated animals compared to vehicle controls. High-throughput sequencing and RNA expression microarray analysis revealed that treatment resulted in decreased expression of inflammatory response genes and increased lung metabolic and repair responses. These results directly demonstrate that 1918 influenza virus infection leads to an immunopathogenic immune response with excessive inflammatory and cell death responses that can be limited by treatment with the catalytic antioxidant EUK-207.
DOI: 10.1016/j.freeradbiomed.2013.10.014
PubMed: 24140866
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Kash</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: kashj@niaid.nih.gov.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Xiao, Yongli" sort="Xiao, Yongli" uniqKey="Xiao Y" first="Yongli" last="Xiao">Yongli Xiao</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Davis, A Sally" sort="Davis, A Sally" uniqKey="Davis A" first="A Sally" last="Davis">A Sally Davis</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Walters, Kathie Anne" sort="Walters, Kathie Anne" uniqKey="Walters K" first="Kathie-Anne" last="Walters">Kathie-Anne Walters</name><affiliation wicri:level="2"><nlm:affiliation>Institute for Systems Biology, Seattle, WA 98109, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Institute for Systems Biology, Seattle, WA 98109</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S" last="Chertow">Daniel S. Chertow</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Easterbrook, Judith D" sort="Easterbrook, Judith D" uniqKey="Easterbrook J" first="Judith D" last="Easterbrook">Judith D. Easterbrook</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Dunfee, Rebecca L" sort="Dunfee, Rebecca L" uniqKey="Dunfee R" first="Rebecca L" last="Dunfee">Rebecca L. Dunfee</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Sandouk, Aline" sort="Sandouk, Aline" uniqKey="Sandouk A" first="Aline" last="Sandouk">Aline Sandouk</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Jagger, Brett W" sort="Jagger, Brett W" uniqKey="Jagger B" first="Brett W" last="Jagger">Brett W. Jagger</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Schwartzman, Louis M" sort="Schwartzman, Louis M" uniqKey="Schwartzman L" first="Louis M" last="Schwartzman">Louis M. Schwartzman</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Kuestner, Rolf E" sort="Kuestner, Rolf E" uniqKey="Kuestner R" first="Rolf E" last="Kuestner">Rolf E. Kuestner</name><affiliation wicri:level="2"><nlm:affiliation>Institute for Systems Biology, Seattle, WA 98109, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Institute for Systems Biology, Seattle, WA 98109</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Wehr, Nancy B" sort="Wehr, Nancy B" uniqKey="Wehr N" first="Nancy B" last="Wehr">Nancy B. Wehr</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Huffman, Karl" sort="Huffman, Karl" uniqKey="Huffman K" first="Karl" last="Huffman">Karl Huffman</name><affiliation wicri:level="2"><nlm:affiliation>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Rosenthal, Rosalind A" sort="Rosenthal, Rosalind A" uniqKey="Rosenthal R" first="Rosalind A" last="Rosenthal">Rosalind A. Rosenthal</name><affiliation wicri:level="2"><nlm:affiliation>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Ozinsky, Adrian" sort="Ozinsky, Adrian" uniqKey="Ozinsky A" first="Adrian" last="Ozinsky">Adrian Ozinsky</name><affiliation wicri:level="2"><nlm:affiliation>Institute for Systems Biology, Seattle, WA 98109, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Institute for Systems Biology, Seattle, WA 98109</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Levine, Rodney L" sort="Levine, Rodney L" uniqKey="Levine R" first="Rodney L" last="Levine">Rodney L. Levine</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Doctrow, Susan R" sort="Doctrow, Susan R" uniqKey="Doctrow S" first="Susan R" last="Doctrow">Susan R. Doctrow</name><affiliation wicri:level="2"><nlm:affiliation>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pulmonary Center, Department of Medicine, Boston University Medical School, Boston, MA 02118</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Taubenberger, Jeffery K" sort="Taubenberger, Jeffery K" uniqKey="Taubenberger J" first="Jeffery K" last="Taubenberger">Jeffery K. Taubenberger</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>8-Hydroxy-2'-Deoxyguanosine</term><term>Animals</term><term>Biomarkers (metabolism)</term><term>Caspase 3 (genetics)</term><term>Caspase 3 (metabolism)</term><term>DNA Repair</term><term>Deoxyguanosine (analogs & derivatives)</term><term>Deoxyguanosine (metabolism)</term><term>Dogs</term><term>Female</term><term>Free Radical Scavengers (pharmacology)</term><term>Gene Expression</term><term>Humans</term><term>Inflammation (drug therapy)</term><term>Inflammation (metabolism)</term><term>Inflammation (mortality)</term><term>Inflammation (virology)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Influenza A Virus, H1N1 Subtype (physiology)</term><term>Influenza Pandemic, 1918-1919</term><term>Lung (drug effects)</term><term>Lung (metabolism)</term><term>Lung (pathology)</term><term>Madin Darby Canine Kidney Cells</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Organometallic Compounds (pharmacology)</term><term>Orthomyxoviridae Infections (drug therapy)</term><term>Orthomyxoviridae Infections (metabolism)</term><term>Orthomyxoviridae Infections (mortality)</term><term>Orthomyxoviridae Infections (virology)</term><term>Reactive Oxygen Species (antagonists & inhibitors)</term><term>Reactive Oxygen Species (metabolism)</term><term>Survival Analysis</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de survie</term><term>Animaux</term><term>Caspase-3 (génétique)</term><term>Caspase-3 (métabolisme)</term><term>Cellules rénales canines Madin-Darby</term><term>Charge virale</term><term>Chiens</term><term>Composés organométalliques (pharmacologie)</term><term>Désoxyguanosine (analogues et dérivés)</term><term>Désoxyguanosine (métabolisme)</term><term>Espèces réactives de l'oxygène (antagonistes et inhibiteurs)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Expression des gènes</term><term>Femelle</term><term>Humains</term><term>Infections à Orthomyxoviridae (mortalité)</term><term>Infections à Orthomyxoviridae (métabolisme)</term><term>Infections à Orthomyxoviridae (traitement médicamenteux)</term><term>Infections à Orthomyxoviridae (virologie)</term><term>Inflammation (mortalité)</term><term>Inflammation (métabolisme)</term><term>Inflammation (traitement médicamenteux)</term><term>Inflammation (virologie)</term><term>Marqueurs biologiques (métabolisme)</term><term>Pandémie de grippe de 1918-1919</term><term>Piégeurs de radicaux libres (pharmacologie)</term><term>Poumon ()</term><term>Poumon (anatomopathologie)</term><term>Poumon (métabolisme)</term><term>Réparation de l'ADN</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Sous-type H1N1 du virus de la grippe A (pathogénicité)</term><term>Sous-type H1N1 du virus de la grippe A (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Deoxyguanosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Caspase 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>Caspase 3</term><term>Deoxyguanosine</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Free Radical Scavengers</term><term>Organometallic Compounds</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>8-Hydroxy-2'-Deoxyguanosine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Désoxyguanosine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Inflammation</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Caspase-3</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Lung</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Inflammation</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Désoxyguanosine</term><term>Espèces réactives de l'oxygène</term><term>Infections à Orthomyxoviridae</term><term>Inflammation</term><term>Marqueurs biologiques</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Composés organométalliques</term><term>Piégeurs de radicaux libres</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Inflammation</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>DNA Repair</term><term>Dogs</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Influenza Pandemic, 1918-1919</term><term>Madin Darby Canine Kidney Cells</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Survival Analysis</term><term>Viral Load</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de survie</term><term>Animaux</term><term>Cellules rénales canines Madin-Darby</term><term>Charge virale</term><term>Chiens</term><term>Expression des gènes</term><term>Femelle</term><term>Humains</term><term>Pandémie de grippe de 1918-1919</term><term>Poumon</term><term>Réparation de l'ADN</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée BALB C</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The 1918 influenza pandemic caused over 40 million deaths worldwide, with 675,000 deaths in the United States alone. Studies in several experimental animal models showed that 1918 influenza virus infection resulted in severe lung pathology associated with dysregulated immune and cell death responses. To determine if reactive oxygen species produced by host inflammatory responses play a central role in promoting severity of lung pathology, we treated 1918 influenza virus-infected mice with the catalytic catalase/superoxide dismutase mimetic, salen-manganese complex EUK-207 beginning 3 days postinfection. Postexposure treatment of mice infected with a lethal dose of the 1918 influenza virus with EUK-207 resulted in significantly increased survival and reduced lung pathology without a reduction in viral titers. In vitro studies also showed that EUK-207 treatment did not affect 1918 influenza viral replication. Immunohistochemical analysis showed a reduction in the detection of the apoptosis marker cleaved caspase-3 and the oxidative stress marker 8-oxo-2'-deoxyguanosine in lungs of EUK-207-treated animals compared to vehicle controls. High-throughput sequencing and RNA expression microarray analysis revealed that treatment resulted in decreased expression of inflammatory response genes and increased lung metabolic and repair responses. These results directly demonstrate that 1918 influenza virus infection leads to an immunopathogenic immune response with excessive inflammatory and cell death responses that can be limited by treatment with the catalytic antioxidant EUK-207. </div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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