Source:http://linkedlifedata.com/resource/pubmed/id/10679099
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2000-3-23
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| pubmed:abstractText |
Innate immunity plays an important role in pulmonary host defense against Pneumocystis carinii, an important pathogen in individuals with impaired cell-mediated immunity. We investigated the role of GM-CSF in host defense in a model of P. carinii pneumonia induced by intratracheal inoculation of CD4-depleted mice. Lung GM-CSF levels increased progressively during the infection and were significantly greater than those in uninfected controls 3, 4, and 5 wk after inoculation. When GM-CSF gene-targeted mice (GM-/-) depleted of CD4+ cells were inoculated with P. carinii, the intensities of infection and inflammation were increased significantly compared with those in CD4-depleted wild-type mice. In contrast, transgenic expression of GM-CSF directed solely in the lungs of GM-/- mice (using the surfactant protein C promoter) dramatically decreased the intensity of infection and inflammation 4 wk after inoculation. The concentrations of surfactant proteins A and D were greater in both uninfected and infected GM-/- mice compared with those in wild-type controls, suggesting that this component of the innate response was preserved in the GM-/- mice. However, alveolar macrophages (AM) from GM-/- mice demonstrated impaired phagocytosis of purified murine P. carinii organisms in vitro compared with AM from wild-type mice. Similarly, AM production of TNF-alpha in response to P. carinii in vitro was totally absent in AM from GM-/- mice, while GM-CSF-replete mice produced abundant TNF in this setting. Thus, GM-CSF plays a critical role in the inflammatory response to P. carinii in the setting of impaired cell-mediated immunity through effects on AM activation.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
164
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2602-9
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:10679099-Animals,
pubmed-meshheading:10679099-Cells, Cultured,
pubmed-meshheading:10679099-Genetic Predisposition to Disease,
pubmed-meshheading:10679099-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:10679099-Immunity, Innate,
pubmed-meshheading:10679099-Lung,
pubmed-meshheading:10679099-Macrophages, Alveolar,
pubmed-meshheading:10679099-Mice,
pubmed-meshheading:10679099-Mice, Inbred BALB C,
pubmed-meshheading:10679099-Mice, Inbred C57BL,
pubmed-meshheading:10679099-Mice, Nude,
pubmed-meshheading:10679099-Mice, Transgenic,
pubmed-meshheading:10679099-Phagocytosis,
pubmed-meshheading:10679099-Pneumocystis,
pubmed-meshheading:10679099-Pneumonia, Pneumocystis,
pubmed-meshheading:10679099-Proteolipids,
pubmed-meshheading:10679099-Pulmonary Surfactants,
pubmed-meshheading:10679099-Tumor Necrosis Factor-alpha
|
| pubmed:year |
2000
|
| pubmed:articleTitle |
Granulocyte-macrophage colony-stimulating factor in the innate immune response to Pneumocystis carinii pneumonia in mice.
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| pubmed:affiliation |
Division of Pulmonary and Critical Care Medicine, University of Michigan, and Department of Veterans Affairs Medical Center, Ann Arbor, MI 48105, USA. rpaine@umich.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.,
Research Support, Non-U.S. Gov't
|