TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation. - Wikidata - thesis-toulmin - TriplyDB

TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation.

TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation.

http://www.wikidata.org/entity/Q33845593

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The Rise and Fall of Hyaluronan in Respiratory Diseases Size Matters: Molecular Weight Specificity of Hyaluronan Effects in Cell Biology Genes of innate immunity and the biological response to inhaled ozone RAGE: a new frontier in chronic airways disease Update in environmental and occupational medicine 2010 The effect of environmental oxidative stress on airway inflammation Association between plasma levels of hyaluronic acid and functional outcome in acute stroke patients.Ozone activates pulmonary dendritic cells and promotes allergic sensitization through a Toll-like receptor 4-dependent mechanism Hyaluronan signaling during ozone-induced lung injury requires TLR4, MyD88, and TIRAP.Prostaglandin E2 reduces Toll-like receptor 4 expression in alveolar macrophages by inhibition of translation.Atopic asthmatic subjects but not atopic subjects without asthma have enhanced inflammatory response to ozone.CD44 deficiency is associated with increased bacterial clearance but enhanced lung inflammation during Gram-negative pneumonia.Augmentation of arginase 1 expression by exposure to air pollution exacerbates the airways hyperresponsiveness in murine models of asthma Nitric oxide mediates relative airway hyporesponsiveness to lipopolysaccharide in surfactant protein A-deficient mice.Mechanical stretch induces epithelial-mesenchymal transition in alveolar epithelia via hyaluronan activation of innate immunity.Resolution of Toll-like receptor 4-mediated acute lung injury is linked to eicosanoids and suppressor of cytokine signaling 3 Effects of air pollutants on innate immunity: the role of Toll-like receptors and nucleotide-binding oligomerization domain-like receptors.Role of hyaluronan and hyaluronan-binding proteins in lung pathobiology.Interaction with epithelial cells modifies airway macrophage response to ozone Hyaluronan fragments as mediators of inflammation in allergic pulmonary disease Ozone inhalation promotes CX3CR1-dependent maturation of resident lung macrophages that limit oxidative stress and inflammation.Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury The role of the extracellular matrix protein mindin in airway response to environmental airways injury Hyaluronan stimulates ex vivo B lymphocyte chemotaxis and cytokine production in a murine model of fungal allergic asthma Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness The lung response to ozone is determined by age and is partially dependent on toll-Like receptor 4.Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.TSG-6 protein is crucial for the development of pulmonary hyaluronan deposition, eosinophilia, and airway hyperresponsiveness in a murine model of asthma.Hyaluronan activation of the Nlrp3 inflammasome contributes to the development of airway hyperresponsiveness.Ozone enhances pulmonary innate immune response to a Toll-like receptor-2 agonist.Extracellular Matrix Protein Mindin is Required for the Complete Allergic Response to Fungal-Associated Proteinase.The role of hyaluronan in the pathobiology and treatment of respiratory disease.CD36 mediates endothelial dysfunction downstream of circulating factors induced by O3 exposure.Ambient ozone and pulmonary innate immunity.Ozone-Induced Hypertussive Responses in Rabbits and Guinea Pigs.Acute Lung Injury Regulation by Hyaluronan.Inhaled birch pollen extract induces airway hyperresponsiveness via oxidative stress but independently of pollen-intrinsic NADPH oxidase activity, or the TLR4-TRIF pathway.The role of oxidative stress and innate immunity in O(3) and endotoxin-induced human allergic airway disease.Novel roles of peroxiredoxins in inflammation, cancer and innate immunity.Potential medications or compounds acting on toll-like receptors in cerebral ischemia.

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P2860

TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation.

http://www.wikidata.org/entity/Q33845593

description

2009 nî lūn-bûn

@nan

2009 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

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TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

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type

label

TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

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TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

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prefLabel

TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

@ast

TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

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RCCM.200903-0381OC

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American Journal of Respiratory and Critical Care Medicine

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TLR4 is necessary for hyaluron ...... veness after ozone inhalation.

@en

P2093

David A Schwartz

http://www.w3.org/2001/XMLSchema#string

Erin N Potts

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James Y Lindsey

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John W Hollingsworth

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Stavros Garantziotis

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Timothy S Blackwell

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Vandy P Stober

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Vasiliy V Polosukhin

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W Michael Foster

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Zhuowei Li

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P2860

LPS-TLR4 signaling to IRF-3/7 and NF-kappaB involves the toll adapters TRAM and TRIF

Health-related benefits of attaining the 8-hr ozone standard

An association between air pollution and mortality in six U.S. cities

A human homologue of the Drosophila Toll protein signals activation of adaptive immunity

Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product

Resolution of lung inflammation by CD44

Ozone exposure of macrophages induces an alveolar epithelial chemokine response through IL-1alpha

Toll-like receptor 4 mediates ozone-induced murine lung hyperpermeability via inducible nitric oxide synthase.

Ozone and short-term mortality in 95 US urban communities, 1987-2000.

Regulation of lung injury and repair by Toll-like receptors and hyaluronan.

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666-675

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10.1164/RCCM.200903-0381OC

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7

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181

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2009-12-10T00:00:00Z

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20007931

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Toll-like receptor

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2868499

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