Source:http://linkedlifedata.com/resource/pubmed/id/11970909
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2002-4-23
|
| 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.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Clodronic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/endotoxin, Escherichia coli
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
1044-1549
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
572-8
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:11970909-Administration, Inhalation,
pubmed-meshheading:11970909-Animals,
pubmed-meshheading:11970909-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:11970909-Cell Count,
pubmed-meshheading:11970909-Clodronic Acid,
pubmed-meshheading:11970909-Cytokines,
pubmed-meshheading:11970909-Disease Models, Animal,
pubmed-meshheading:11970909-Endotoxins,
pubmed-meshheading:11970909-Injections, Intraperitoneal,
pubmed-meshheading:11970909-Injections, Intravenous,
pubmed-meshheading:11970909-Instillation, Drug,
pubmed-meshheading:11970909-Intubation, Intratracheal,
pubmed-meshheading:11970909-Lipopolysaccharides,
pubmed-meshheading:11970909-Lung,
pubmed-meshheading:11970909-Macrophages, Alveolar,
pubmed-meshheading:11970909-Mice,
pubmed-meshheading:11970909-Mice, Inbred C57BL,
pubmed-meshheading:11970909-NF-kappa B,
pubmed-meshheading:11970909-Neutrophils,
pubmed-meshheading:11970909-Pneumonia
|
| pubmed:year |
2002
|
| pubmed:articleTitle |
Macrophages are necessary for maximal nuclear factor-kappa B activation in response to endotoxin.
|
| pubmed:affiliation |
Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2650, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|