Source:http://linkedlifedata.com/resource/pubmed/id/12376348
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2002-10-11
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pubmed:abstractText |
We investigated the role of neutrophils in the development of endotoxin-induced airway disease via systemic neutrophil depletion of C3H/HeBFeJ mice and coincident inhalation challenge with lipopolysaccharide (LPS) over a 4-wk period. Mice were made neutropenic with intraperitoneal injections of neutrophil antiserum before and throughout the exposure period. Experimental conditions included LPS-exposed, antiserum-treated; LPS-exposed, control serum-treated; air-exposed, antiserum-treated; and air-exposed, control serum-treated groups. Physiological, biological, and morphological assessments were performed after a 4-wk exposure and again after a 4-wk recovery period. After the 4-wk exposure, LPS-induced inflammation of the lower airways was significantly attenuated in the neutropenic mice, although airway responsiveness (AR) to methacholine (MCh) remained unchanged. After the recovery period, LPS-exposed neutrophil-replete mice had increased AR to MCh when compared with the LPS-exposed neutropenic animals. Morphometric data indicate that the 4-wk exposure to LPS leads to a substantial expansion of the subepithelial area of the medium-sized airways (90-129 microm diameter) in nonneutropenic mice but not neutropenic mice, and this difference persisted even after the recovery period. Expression of bronchial epithelial and subepithelial transforming growth factor-beta1 (TGF-beta1) was diminished in the challenged neutropenic mice compared with the neutrophil-sufficient mice. These studies demonstrate that neutrophils play a critical role in the development of chronic LPS-induced airway disease.
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pubmed:grant | |
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 |
Nov
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pubmed:issn |
1040-0605
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
283
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
L952-62
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12376348-Animals,
pubmed-meshheading:12376348-Bronchial Hyperreactivity,
pubmed-meshheading:12376348-Disease Models, Animal,
pubmed-meshheading:12376348-Endotoxins,
pubmed-meshheading:12376348-Escherichia coli,
pubmed-meshheading:12376348-Lipopolysaccharides,
pubmed-meshheading:12376348-Male,
pubmed-meshheading:12376348-Mice,
pubmed-meshheading:12376348-Mice, Inbred C3H,
pubmed-meshheading:12376348-Neutrophils,
pubmed-meshheading:12376348-Time Factors
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pubmed:year |
2002
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pubmed:articleTitle |
Neutrophils play a critical role in development of LPS-induced airway disease.
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pubmed:affiliation |
Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center and Veterans Affairs Medical Center, Durham, North Carolina 27710, USA. jsavov@acpub.duke.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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