Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.
Identifieur interne : 000F63 ( Main/Merge ); précédent : 000F62; suivant : 000F64Ability of recombinant human catalase to suppress inflammation of the murine lung induced by influenza A.
Auteurs : Xunlong Shi [République populaire de Chine] ; Zhihui Shi ; Hai Huang ; Hongguang Zhu ; Pei Zhou ; Haiyan Zhu ; Dianwen JuSource :
- Inflammation [ 1573-2576 ] ; 2014.
Descripteurs français
- KwdFr :
- ARN messager (génétique), Activation des macrophages (), Animaux, Attribution aléatoire, Catalase (génétique), Catalase (pharmacologie), Cytokines (biosynthèse), Cytokines (génétique), Cytokines (sang), Espèces réactives de l'oxygène (métabolisme), Granulocytes neutrophiles (immunologie), Humains, Infections à Orthomyxoviridae (traitement médicamenteux), Infiltration par les neutrophiles (), Inflammation (traitement médicamenteux), Macrophages (immunologie), Malonaldéhyde (métabolisme), Mâle, Pneumopathie virale (traitement médicamenteux), Poumon (anatomopathologie), Protéines recombinantes (génétique), Protéines recombinantes (pharmacologie), Souris, Souris de lignée ICR, Sous-type H1N1 du virus de la grippe A (pathogénicité), Stress oxydatif (immunologie), Transduction du signal (immunologie).
- MESH :
- anatomopathologie : Poumon.
- biosynthèse : Cytokines.
- génétique : ARN messager, Catalase, Cytokines, Protéines recombinantes.
- immunologie : Granulocytes neutrophiles, Macrophages, Stress oxydatif, Transduction du signal.
- métabolisme : Espèces réactives de l'oxygène, Malonaldéhyde.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- pharmacologie : Catalase, Protéines recombinantes.
- sang : Cytokines.
- traitement médicamenteux : Infections à Orthomyxoviridae, Inflammation, Pneumopathie virale.
- Activation des macrophages, Animaux, Attribution aléatoire, Humains, Infiltration par les neutrophiles, Mâle, Souris, Souris de lignée ICR.
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
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pubmed:24385240Le document en format XML
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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="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>Activation des macrophages ()</term><term>Animaux</term><term>Attribution aléatoire</term><term>Catalase (génétique)</term><term>Catalase (pharmacologie)</term><term>Cytokines (biosynthèse)</term><term>Cytokines (génétique)</term><term>Cytokines (sang)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Granulocytes neutrophiles (immunologie)</term><term>Humains</term><term>Infections à Orthomyxoviridae (traitement médicamenteux)</term><term>Infiltration par les neutrophiles ()</term><term>Inflammation (traitement médicamenteux)</term><term>Macrophages (immunologie)</term><term>Malonaldéhyde 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xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Inflammation</term><term>Pneumopathie virale</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><keywords scheme="MESH" xml:lang="fr"><term>Activation des macrophages</term><term>Animaux</term><term>Attribution aléatoire</term><term>Humains</term><term>Infiltration par les neutrophiles</term><term>Mâle</term><term>Souris</term><term>Souris de lignée ICR</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></record>Pour manipuler ce document sous Unix (Dilib)
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