| pubmed-article:12376348 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C0699949 | lld:lifeskim |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:12376348 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:12376348 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:12376348 | pubmed:dateCreated | 2002-10-11 | lld:pubmed |
| pubmed-article:12376348 | 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. | lld:pubmed |
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| pubmed-article:12376348 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12376348 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12376348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12376348 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12376348 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:12376348 | pubmed:issn | 1040-0605 | lld:pubmed |
| pubmed-article:12376348 | pubmed:author | pubmed-author:SchwartzDavid... | lld:pubmed |
| pubmed-article:12376348 | pubmed:author | pubmed-author:CostaDaniel... | lld:pubmed |
| pubmed-article:12376348 | pubmed:author | pubmed-author:BrassDavid... | lld:pubmed |
| pubmed-article:12376348 | pubmed:author | pubmed-author:SavovJordan... | lld:pubmed |
| pubmed-article:12376348 | pubmed:author | pubmed-author:GavettStephen... | lld:pubmed |
| pubmed-article:12376348 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12376348 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:12376348 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12376348 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12376348 | pubmed:pagination | L952-62 | lld:pubmed |
| pubmed-article:12376348 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:meshHeading | pubmed-meshheading:12376348... | lld:pubmed |
| pubmed-article:12376348 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12376348 | pubmed:articleTitle | Neutrophils play a critical role in development of LPS-induced airway disease. | lld:pubmed |
| pubmed-article:12376348 | 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 | lld:pubmed |
| pubmed-article:12376348 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12376348 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12376348 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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