Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages.
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Microbial Ligand Costimulation Drives Neutrophilic Steroid-Refractory AsthmaCarbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liverTranscriptomic analysis of the temporal host response to skin infestation with the ectoparasitic mite Psoroptes ovisDifferences in inflammation and acute phase response but similar genotoxicity in mice following pulmonary exposure to graphene oxide and reduced graphene oxide.Concomitant exposure to ovalbumin and endotoxin augments airway inflammation but not airway hyperresponsiveness in a murine model of asthma.Haemophilus influenzae infection drives IL-17-mediated neutrophilic allergic airways diseaseSevoflurane inhibits nuclear factor-κB activation in lipopolysaccharide-induced acute inflammatory lung injury via toll-like receptor 4 signaling.Associations of allergic sensitization and clinical phenotypes with innate immune response genes polymorphisms are modified by house dust mite allergen exposure.Antagonism of the histamine H4 receptor reduces LPS-induced TNF production in vivo.Blockade of Airway Inflammation by Kaempferol via Disturbing Tyk-STAT Signaling in Airway Epithelial Cells and in Asthmatic MiceT cells suppress memory-dependent rapid mucous cell metaplasia in mouse airways.The Hapten-Atopy hypothesis II: the 'cutaneous hapten paradox'.The hapten-atopy hypothesis III: the potential role of airborne chemicals.Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics.Interaction Between Helminths and Toll-Like Receptors: Possibilities and Potentials for Asthma Therapy.LPS exacerbates functional and inflammatory responses to ovalbumin and decreases sensitivity to inhaled fluticasone propionate in a guinea pig model of asthmaProtective effect of suppressing STAT3 activity in LPS-induced acute lung injuryTRPM2 channels are not required for acute airway inflammation in OVA-induced severe allergic asthma in mice.Differential regulation of inflammation and immunity in mild and severe experimental asthma.A toll-like receptor 4 (TLR4) variant is associated with asthma severity.Establishment of a mouse model of lipopolysaccharide-induced neutrophilic nasal polyps.Mast cells and sphingosine-1-phosphate underlie prelesional remodeling in a mouse model of eczema.Modulation of the IL-23/IL-17 axis by fenofibrate ameliorates the ovalbumin/lipopolysaccharide-induced airway inflammation and bronchial asthma in rats.The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation.Dual Role of Toll-like Receptors in Human and Experimental Asthma Models.
P2860
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P2860
Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages.
description
2009 nî lūn-bûn
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2009年の論文
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2009年学术文章
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2009年学术文章
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2009年学术文章
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2009年学术文章
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name
Different doses of lipopolysac ...... thway in alveolar macrophages.
@en
Different doses of lipopolysac ...... thway in alveolar macrophages.
@nl
type
label
Different doses of lipopolysac ...... thway in alveolar macrophages.
@en
Different doses of lipopolysac ...... thway in alveolar macrophages.
@nl
prefLabel
Different doses of lipopolysac ...... thway in alveolar macrophages.
@en
Different doses of lipopolysac ...... thway in alveolar macrophages.
@nl
P2093
P2860
P921
P1433
P1476
Different doses of lipopolysac ...... thway in alveolar macrophages.
@en
P2093
Hongjia Li
Shujuan Wang
P2860
P304
P356
10.1080/02770900802610050
P407
P50
P577
2009-04-01T00:00:00Z