An absence of reactive oxygen species improves the resolution of lung influenza infection. - Wikidata - wikimedia - TriplyDB

An absence of reactive oxygen species improves the resolution of lung influenza infection.

An absence of reactive oxygen species improves the resolution of lung influenza infection.

http://www.wikidata.org/entity/Q30354387

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Inhibition of Nox2 oxidase activity ameliorates influenza A virus-induced lung inflammation The host immune response in respiratory virus infection: balancing virus clearance and immunopathology.NADPH oxidases in lung health and disease Innate immunity to influenza virus: implications for future therapy NADPH oxidase-1 plays a crucial role in hyperoxia-induced acute lung injury in mice A Role for Neutrophils in Viral Respiratory Disease.Treatment with the reactive oxygen species scavenger EUK-207 reduces lung damage and increases survival during 1918 influenza virus infection in mice T cell responses during influenza infection: getting and keeping control.Genome-wide association study identifies nox3 as a critical gene for susceptibility to noise-induced hearing loss.Possible roles of proinflammatory and chemoattractive cytokines produced by human fetal membrane cells in the pathology of adverse pregnancy outcomes associated with influenza virus infection.Inducible nitric oxide contributes to viral pathogenesis following highly pathogenic influenza virus infection in mice.Requirement of NOX2 and reactive oxygen species for efficient RIG-I-mediated antiviral response through regulation of MAVS expression.NOX enzymes and pulmonary disease.The Induction of Pattern-Recognition Receptor Expression against Influenza A Virus through Duox2-Derived Reactive Oxygen Species in Nasal Mucosa Reactive oxygen species induce antiviral innate immune response through IFN-λ regulation in human nasal epithelial cells.Pulmonary endothelial cell NOX IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia.Endosomal NOX2 oxidase exacerbates virus pathogenicity and is a target for antiviral therapy.CD11b⁺, Ly6G⁺ cells produce type I interferon and exhibit tissue protective properties following peripheral virus infection An oxidative environment promotes growth of Mycobacterium abscessus.Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress.Genetic ablation of phagocytic NADPH oxidase in mice limits TNFα-induced inflammation in the lungs but not other tissues.Rhinovirus-induced barrier dysfunction in polarized airway epithelial cells is mediated by NADPH oxidase 1.H5N1 influenza virus pathogenesis in genetically diverse mice is mediated at the level of viral load.NADPH oxidase deficiency regulates Th lineage commitment and modulates autoimmunity.Expression of suppressor of cytokine signaling 1 (SOCS1) impairs viral clearance and exacerbates lung injury during influenza infection.NADPH Oxidase 1 Is Associated with Altered Host Survival and T Cell Phenotypes after Influenza A Virus Infection in Mice NOX Modifiers-Just a Step Away from Application in the Therapy of Airway Inflammation?Ebselen and congeners inhibit NADPH oxidase 2-dependent superoxide generation by interrupting the binding of regulatory subunits.NADPH oxidases: an overview from structure to innate immunity-associated pathologies.Redox homeostasis, T cells and kidney diseases: three faces in the dark.NADPH oxidases in lung biology and pathology: host defense enzymes, and more.Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration.CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and -independent mechanisms.Decreased STAT5 phosphorylation and GATA-3 expression in NOX2-deficient T cells: role in T helper development Role of NADPH phagocyte oxidase in host defense against acute respiratory Acinetobacter baumannii infection in mice.Genome-wide fitness profiling reveals adaptations required by Haemophilus in coinfection with influenza A virus in the murine lung.Nox2-derived oxidative stress results in inefficacy of antibiotics against post-influenza S. aureus pneumonia.The antioxidant mimetic, MnTE-2-PyP, reduces intracellular growth of Mycobacterium abscessus.Innate immune control and regulation of influenza virus infections.

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P2860

An absence of reactive oxygen species improves the resolution of lung influenza infection.

http://www.wikidata.org/entity/Q30354387

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2006 nî lūn-bûn

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2006年の論文

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An absence of reactive oxygen ...... n of lung influenza infection.

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European Journal of Immunology

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An absence of reactive oxygen ...... n of lung influenza infection.

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Aaron J Rae

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Lorna Edwards

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Robert J Snelgrove

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P2860

Interactions between cytosolic components of the NADPH oxidase: p40phox interacts with both p67phox and p47phox.

Interferons induce xanthine dehydrogenase gene expression in L929 cells

Oxygen free radicals as pathogenic molecules in viral diseases.

Influenza viruses, cell enzymes, and pathogenicity.

Role of NADPH oxidase in the mechanism of lung neutrophil sequestration and microvessel injury induced by Gram-negative sepsis: studies in p47phox-/- and gp91phox-/- mice.

p47phox deficiency impairs NF-kappa B activation and host defense in Pseudomonas pneumonia.

Temporal segregation of 4-1BB versus CD28-mediated costimulation: 4-1BB ligand influences T cell numbers late in the primary response and regulates the size of the T cell memory response following influenza infection.

Cutting edge: pulmonary immunopathology mediated by antigen-specific expression of TNF-alpha by antiviral CD8+ T cells.

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1364-1373

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10.1002/EJI.200635977

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36

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16703568

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