| pubmed-article:11970909 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11970909 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:11970909 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:11970909 | lifeskim:mentions | umls-concept:C2752174 | lld:lifeskim |
| pubmed-article:11970909 | lifeskim:mentions | umls-concept:C0205289 | lld:lifeskim |
| pubmed-article:11970909 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11970909 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11970909 | pubmed:dateCreated | 2002-4-23 | lld:pubmed |
| pubmed-article:11970909 | pubmed:abstractText | To define the role of macrophages in regulating the lung's response to Escherichia coli endotoxin (lipopolysaccharide [LPS]), depletion of macrophages was accomplished by administration of dichloromethylene diphosphonate (clodronate) delivered via intratracheal (i.t.) and/or intravenous (i.v.) routes. Clodronate reduced the number of macrophages in lung lavage 48 h after either i.t. or i.v. administration, but combined i.t. + i.v. clodronate achieved the most profound depletion (90%). Although i.t. clodronate alone had little effect on the evolution of lung inflammation, combined i.t. + i.v. clodronate treatment decreased neutrophilic alveolitis 4 h after exposure to aerosolized LPS by 80% compared with mice treated with empty liposomes. This decrease was associated with impaired activation of nuclear factor (NF)-kappa B and lower concentrations of tumor necrosis factor (TNF)-alpha in lung lavage fluid. Combined i.t. + i.v. clodronate markedly reduced lung NF-kappa B activation and the intensity of neutrophilic alveolitis after intraperitoneal (i.p.) LPS; however, i.v. clodronate alone had no effect on NF-kappa B activation in either liver or lung tissue or the development of neutrophilic alveolitis. We conclude that generalized macrophage depletion reduces NF-kappa B activation, generation of cytokines, and neutrophilic lung inflammation in response to gram negative bacterial endotoxin. These findings define the role of the macrophage as a critical component for initiation of the NF-kappa B-dependent innate immune response. | lld:pubmed |
| pubmed-article:11970909 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11970909 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11970909 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11970909 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11970909 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11970909 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11970909 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11970909 | pubmed:month | May | lld:pubmed |
| pubmed-article:11970909 | pubmed:issn | 1044-1549 | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:GaoXiangX | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:ChristmanJohn... | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:KoayM... | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:WashingtonMar... | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:ParmanKelly... | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:SadikotRuxana... | lld:pubmed |
| pubmed-article:11970909 | pubmed:author | pubmed-author:BlackwellTimo... | lld:pubmed |
| pubmed-article:11970909 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11970909 | pubmed:volume | 26 | lld:pubmed |
| pubmed-article:11970909 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11970909 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11970909 | pubmed:pagination | 572-8 | lld:pubmed |
| pubmed-article:11970909 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11970909 | pubmed:meshHeading | pubmed-meshheading:11970909... | lld:pubmed |
| pubmed-article:11970909 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11970909 | pubmed:articleTitle | Macrophages are necessary for maximal nuclear factor-kappa B activation in response to endotoxin. | lld:pubmed |
| pubmed-article:11970909 | pubmed:affiliation | Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2650, USA. | lld:pubmed |
| pubmed-article:11970909 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11970909 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11970909 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:11970909 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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