Source:http://linkedlifedata.com/resource/pubmed/id/10830775
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2000-6-8
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pubmed:abstractText |
To study pathogenetic mechanisms in chronic asthma, we employed a novel experimental model that replicates characteristic features of the human disease. Chronic inflammation and epithelial changes, specifically localized to the airways, were induced by repeated exposure of systemically sensitized BALB/c mice to low mass concentrations of aerosolized ovalbumin for 6 weeks. The contribution of Th2 cytokine-driven inflammation to the development of airway lesions and hyperreactivity was assessed in cytokine-deficient mice. In interleukin-5-deficient animals, intraepithelial eosinophils and chronic inflammatory cells in the lamina propria of the airways were markedly decreased; however, these animals developed epithelial hypertrophy and subepithelial fibrosis comparable with that observed in sensitized wild type mice. Airway hyperreactivity to inhaled methacholine did not develop in interleukin-5-deficient mice. In contrast, interleukin-4-deficient mice exhibited no decrease in airway inflammation, but had significantly greater epithelial hypertrophy and subepithelial fibrosis, as well as exaggerated hyperreactivity to methacholine. We conclude that interleukin-5, but not interleukin-4, plays a central role in the development of chronic inflammation of the airways and the induction of airway hyperreactivity. Furthermore, chronic epithelial and fibrotic changes occur independently of interleukin-5 and are not required for the development of airway hyperreactivity. The dissociation between airway wall remodeling and airway hyperreactivity has important implications for therapeutic approaches to chronic asthma.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0023-6837
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
80
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
655-62
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:10830775-Animals,
pubmed-meshheading:10830775-Asthma,
pubmed-meshheading:10830775-Cell Movement,
pubmed-meshheading:10830775-Chronic Disease,
pubmed-meshheading:10830775-Disease Models, Animal,
pubmed-meshheading:10830775-Epithelium,
pubmed-meshheading:10830775-Female,
pubmed-meshheading:10830775-Fibrosis,
pubmed-meshheading:10830775-Hypertrophy,
pubmed-meshheading:10830775-Inflammation,
pubmed-meshheading:10830775-Interleukin-4,
pubmed-meshheading:10830775-Interleukin-5,
pubmed-meshheading:10830775-Mice,
pubmed-meshheading:10830775-Mice, Inbred BALB C,
pubmed-meshheading:10830775-Neutrophils
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pubmed:year |
2000
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pubmed:articleTitle |
Dissociation of inflammatory and epithelial responses in a murine model of chronic asthma.
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pubmed:affiliation |
Division of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Canberra. Paul.Foster@anu.edu.au
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pubmed:publicationType |
Journal Article
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