Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.
Identifieur interne : 000496 ( PubMed/Corpus ); précédent : 000495; suivant : 000497Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.
Auteurs : Xunlong Shi ; Zhihui Shi ; Hai Huang ; Hongguang Zhu ; Pei Zhou ; Haiyan Zhu ; Dianwen JuSource :
- Inflammation [ 1573-2576 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Catalase (genetics), Catalase (pharmacology), Cytokines (biosynthesis), Cytokines (blood), Cytokines (genetics), Humans, Inflammation (drug therapy), Influenza A Virus, H1N1 Subtype (pathogenicity), Lung (pathology), Macrophage Activation (drug effects), Macrophages (immunology), Male, Malondialdehyde (metabolism), Mice, Mice, Inbred ICR, Neutrophil Infiltration (drug effects), Neutrophils (immunology), Orthomyxoviridae Infections (drug therapy), Oxidative Stress (immunology), Pneumonia, Viral (drug therapy), RNA, Messenger (genetics), Random Allocation, Reactive Oxygen Species (metabolism), Recombinant Proteins (genetics), Recombinant Proteins (pharmacology), Signal Transduction (immunology).
- MESH :
- chemical , biosynthesis : Cytokines.
- chemical , blood : Cytokines.
- chemical , genetics : Catalase, Cytokines, RNA, Messenger, Recombinant Proteins.
- chemical , metabolism : Malondialdehyde, Reactive Oxygen Species.
- chemical , pharmacology : Catalase, Recombinant Proteins.
- drug effects : Macrophage Activation, Neutrophil Infiltration.
- drug therapy : Inflammation, Orthomyxoviridae Infections, Pneumonia, Viral.
- immunology : Macrophages, Neutrophils, Oxidative Stress, Signal Transduction.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- pathology : Lung.
- Animals, Humans, Male, Mice, Mice, Inbred ICR, Random Allocation.
Abstract
Influenza A virus pandemics and emerging antiviral resistance highlight the urgent need for novel generic pharmacological strategies that reduce both viral replication and inflammation of the lung. We have previously investigated the therapeutic efficacy of recombinant human catalase (rhCAT) against viral pneumonia in mice, but the protection mechanisms involved were not explored. In the present study, we have performed a more in-depth analysis covering survival, lung inflammation, immune cell responses, production of cytokines, and inflammation signaling pathways in mice. Male imprinting control region mice were infected intranasally with high pathogenicity (H1N1) influenza A virus followed by treatment with recombinant human catalase. The administration of rhCAT resulted in a significant reduction in inflammatory cell infiltration (e.g., macrophages and neutrophils), inflammatory cytokine levels (e.g., IL-2, IL-6, TNF-α, IFN-γ), the level of the intercellular adhesion molecule 1 chemokine and the mRNA levels of toll-like receptors TLR-4, TLR-7, and NF-κB, as well as partially maintaining the activity of the antioxidant enzymes system. These findings indicated that rhCAT might play a key protective role in viral pneumonia of mice via suppression of inflammatory immune responses.
DOI: 10.1007/s10753-013-9800-2
PubMed: 24385240
Links to Exploration step
pubmed:24385240Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.</title><author><name sortKey="Shi, Xunlong" sort="Shi, Xunlong" uniqKey="Shi X" first="Xunlong" last="Shi">Xunlong Shi</name><affiliation><nlm:affiliation>Department of Drug Biosynthesis, School of Pharmacy, Fudan University, 826 Zhang Heng Road, Shanghai, 201203, China, xunlongshi@fudan.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Shi, Zhihui" sort="Shi, Zhihui" uniqKey="Shi Z" first="Zhihui" last="Shi">Zhihui Shi</name></author><author><name sortKey="Huang, Hai" sort="Huang, Hai" uniqKey="Huang H" first="Hai" last="Huang">Hai Huang</name></author><author><name sortKey="Zhu, Hongguang" sort="Zhu, Hongguang" uniqKey="Zhu H" first="Hongguang" last="Zhu">Hongguang Zhu</name></author><author><name sortKey="Zhou, Pei" sort="Zhou, Pei" uniqKey="Zhou P" first="Pei" last="Zhou">Pei Zhou</name></author><author><name sortKey="Zhu, Haiyan" sort="Zhu, Haiyan" uniqKey="Zhu H" first="Haiyan" last="Zhu">Haiyan Zhu</name></author><author><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24385240</idno><idno type="pmid">24385240</idno><idno type="doi">10.1007/s10753-013-9800-2</idno><idno type="wicri:Area/PubMed/Corpus">000496</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000496</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.</title><author><name sortKey="Shi, Xunlong" sort="Shi, Xunlong" uniqKey="Shi X" first="Xunlong" last="Shi">Xunlong Shi</name><affiliation><nlm:affiliation>Department of Drug Biosynthesis, School of Pharmacy, Fudan University, 826 Zhang Heng Road, Shanghai, 201203, China, xunlongshi@fudan.edu.cn.</nlm:affiliation></affiliation></author><author><name sortKey="Shi, Zhihui" sort="Shi, Zhihui" uniqKey="Shi Z" first="Zhihui" last="Shi">Zhihui Shi</name></author><author><name sortKey="Huang, Hai" sort="Huang, Hai" uniqKey="Huang H" first="Hai" last="Huang">Hai Huang</name></author><author><name sortKey="Zhu, Hongguang" sort="Zhu, Hongguang" uniqKey="Zhu H" first="Hongguang" last="Zhu">Hongguang Zhu</name></author><author><name sortKey="Zhou, Pei" sort="Zhou, Pei" uniqKey="Zhou P" first="Pei" last="Zhou">Pei Zhou</name></author><author><name sortKey="Zhu, Haiyan" sort="Zhu, Haiyan" uniqKey="Zhu H" first="Haiyan" last="Zhu">Haiyan Zhu</name></author><author><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name></author></analytic><series><title level="j">Inflammation</title><idno type="eISSN">1573-2576</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Catalase (genetics)</term><term>Catalase (pharmacology)</term><term>Cytokines (biosynthesis)</term><term>Cytokines (blood)</term><term>Cytokines (genetics)</term><term>Humans</term><term>Inflammation (drug therapy)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Lung (pathology)</term><term>Macrophage Activation (drug effects)</term><term>Macrophages (immunology)</term><term>Male</term><term>Malondialdehyde (metabolism)</term><term>Mice</term><term>Mice, Inbred ICR</term><term>Neutrophil Infiltration (drug effects)</term><term>Neutrophils (immunology)</term><term>Orthomyxoviridae Infections (drug therapy)</term><term>Oxidative Stress (immunology)</term><term>Pneumonia, Viral (drug therapy)</term><term>RNA, Messenger (genetics)</term><term>Random Allocation</term><term>Reactive Oxygen Species (metabolism)</term><term>Recombinant Proteins (genetics)</term><term>Recombinant Proteins (pharmacology)</term><term>Signal Transduction (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Catalase</term><term>Cytokines</term><term>RNA, Messenger</term><term>Recombinant Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Malondialdehyde</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Catalase</term><term>Recombinant Proteins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophage Activation</term><term>Neutrophil Infiltration</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Inflammation</term><term>Orthomyxoviridae Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages</term><term>Neutrophils</term><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred ICR</term><term>Random Allocation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza A virus pandemics and emerging antiviral resistance highlight the urgent need for novel generic pharmacological strategies that reduce both viral replication and inflammation of the lung. We have previously investigated the therapeutic efficacy of recombinant human catalase (rhCAT) against viral pneumonia in mice, but the protection mechanisms involved were not explored. In the present study, we have performed a more in-depth analysis covering survival, lung inflammation, immune cell responses, production of cytokines, and inflammation signaling pathways in mice. Male imprinting control region mice were infected intranasally with high pathogenicity (H1N1) influenza A virus followed by treatment with recombinant human catalase. The administration of rhCAT resulted in a significant reduction in inflammatory cell infiltration (e.g., macrophages and neutrophils), inflammatory cytokine levels (e.g., IL-2, IL-6, TNF-α, IFN-γ), the level of the intercellular adhesion molecule 1 chemokine and the mRNA levels of toll-like receptors TLR-4, TLR-7, and NF-κB, as well as partially maintaining the activity of the antioxidant enzymes system. These findings indicated that rhCAT might play a key protective role in viral pneumonia of mice via suppression of inflammatory immune responses. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24385240</PMID><DateCompleted><Year>2015</Year><Month>06</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-2576</ISSN><JournalIssue CitedMedium="Internet"><Volume>37</Volume><Issue>3</Issue><PubDate><Year>2014</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Inflammation</Title><ISOAbbreviation>Inflammation</ISOAbbreviation></Journal><ArticleTitle>Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.</ArticleTitle><Pagination><MedlinePgn>809-17</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10753-013-9800-2</ELocationID><Abstract><AbstractText>Influenza A virus pandemics and emerging antiviral resistance highlight the urgent need for novel generic pharmacological strategies that reduce both viral replication and inflammation of the lung. We have previously investigated the therapeutic efficacy of recombinant human catalase (rhCAT) against viral pneumonia in mice, but the protection mechanisms involved were not explored. In the present study, we have performed a more in-depth analysis covering survival, lung inflammation, immune cell responses, production of cytokines, and inflammation signaling pathways in mice. Male imprinting control region mice were infected intranasally with high pathogenicity (H1N1) influenza A virus followed by treatment with recombinant human catalase. The administration of rhCAT resulted in a significant reduction in inflammatory cell infiltration (e.g., macrophages and neutrophils), inflammatory cytokine levels (e.g., IL-2, IL-6, TNF-α, IFN-γ), the level of the intercellular adhesion molecule 1 chemokine and the mRNA levels of toll-like receptors TLR-4, TLR-7, and NF-κB, as well as partially maintaining the activity of the antioxidant enzymes system. 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ValidYN="Y"><LastName>Zhu</LastName><ForeName>Haiyan</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Ju</LastName><ForeName>Dianwen</ForeName><Initials>D</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Inflammation</MedlineTA><NlmUniqueID>7600105</NlmUniqueID><ISSNLinking>0360-3997</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen 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