StressCovidV1, PubMed, Corpus, bibRecord, 000503

Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.

Identifieur interne : 000503 ( PubMed/Corpus ); précédent : 000502; suivant : 000504

Treatment 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 ; Yongli Xiao ; A Sally Davis ; Kathie-Anne Walters ; Daniel S. Chertow ; Judith D. Easterbrook ; Rebecca L. Dunfee ; Aline Sandouk ; Brett W. Jagger ; Louis M. Schwartzman ; Rolf E. Kuestner ; Nancy B. Wehr ; Karl Huffman ; Rosalind A. Rosenthal ; Adrian Ozinsky ; Rodney L. Levine ; Susan R. Doctrow ; Jeffery K. Taubenberger

Source :

Free radical biology & medicine [ 1873-4596 ] ; 2014.

RBID : pubmed:24140866

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

Links to Exploration step

pubmed:24140866

Le document en format XML

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<author><name sortKey="Xiao, Yongli" sort="Xiao, Yongli" uniqKey="Xiao Y" first="Yongli" last="Xiao">Yongli Xiao</name>
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<author><name sortKey="Rosenthal, Rosalind A" sort="Rosenthal, Rosalind A" uniqKey="Rosenthal R" first="Rosalind A" last="Rosenthal">Rosalind A. Rosenthal</name>
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</affiliation>
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<author><name sortKey="Ozinsky, Adrian" sort="Ozinsky, Adrian" uniqKey="Ozinsky A" first="Adrian" last="Ozinsky">Adrian Ozinsky</name>
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</affiliation>
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</affiliation>
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</affiliation>
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<author><name sortKey="Schwartzman, Louis M" sort="Schwartzman, Louis M" uniqKey="Schwartzman L" first="Louis M" last="Schwartzman">Louis M. Schwartzman</name>
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</affiliation>
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<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>
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<term>Gene Expression</term>
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<term>Inflammation (metabolism)</term>
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<term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term>
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<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>
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<DateCompleted><Year>2015</Year>
<Month>01</Month>
<Day>06</Day>
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<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
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<Title>Free radical biology & medicine</Title>
<ISOAbbreviation>Free Radic. Biol. Med.</ISOAbbreviation>
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<ArticleTitle>Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.</ArticleTitle>
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<Abstract><AbstractText>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. </AbstractText>
<CopyrightInformation>Published by Elsevier Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kash</LastName>
<ForeName>John C</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><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.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xiao</LastName>
<ForeName>Yongli</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Davis</LastName>
<ForeName>A Sally</ForeName>
<Initials>AS</Initials>
<AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.</Affiliation>
</AffiliationInfo>
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   |texte=   Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.
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Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.

Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice.

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