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
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<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>
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