Source:http://linkedlifedata.com/resource/pubmed/id/14607941
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2003-11-10
|
| pubmed:abstractText |
The role of alveolar macrophages (AM) in host defense against pulmonary infection has been difficult to establish using in vivo models. This may reflect a reliance on models of fulminant infection. To establish a unique model of resolving infection, with which to address the function of AM, C57BL/6 mice received low-dose intratracheal administration of pneumococci. Administration of low doses of pneumococci produced a resolving model of pulmonary infection characterized by clearance of bacteria without features of pneumonia. AM depletion in this model significantly increased bacterial outgrowth in the lung. Interestingly, a significant increase in the number of apoptotic AM was noted with the low-dose infection as compared with mock infection. Caspase inhibition in this model decreased AM apoptosis and increased the number of bacteremic mice, indicating a novel role for caspase activation in pulmonary innate defense against pneumococci. These results suggest that AM play a key role in clearance of bacteria from the lung during subclinical infection and that induction of AM apoptosis contributes to the microbiologic host defense against pneumococci.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amino Acid Chloromethyl Ketones,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/benzyloxycarbonylvalyl-alanyl-aspart...
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
|
| pubmed:volume |
171
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5380-8
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:14607941-Amino Acid Chloromethyl Ketones,
pubmed-meshheading:14607941-Animals,
pubmed-meshheading:14607941-Apoptosis,
pubmed-meshheading:14607941-Bacteremia,
pubmed-meshheading:14607941-Caspases,
pubmed-meshheading:14607941-Cell Count,
pubmed-meshheading:14607941-Cysteine Proteinase Inhibitors,
pubmed-meshheading:14607941-Disease Models, Animal,
pubmed-meshheading:14607941-Dose-Response Relationship, Immunologic,
pubmed-meshheading:14607941-Female,
pubmed-meshheading:14607941-Immunity, Innate,
pubmed-meshheading:14607941-Injections, Intraperitoneal,
pubmed-meshheading:14607941-Intubation, Intratracheal,
pubmed-meshheading:14607941-Macrophages, Alveolar,
pubmed-meshheading:14607941-Mice,
pubmed-meshheading:14607941-Mice, Inbred C57BL,
pubmed-meshheading:14607941-Pneumonia, Pneumococcal,
pubmed-meshheading:14607941-Streptococcus pneumoniae,
pubmed-meshheading:14607941-Up-Regulation
|
| pubmed:year |
2003
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| pubmed:articleTitle |
Alveolar macrophage apoptosis contributes to pneumococcal clearance in a resolving model of pulmonary infection.
|
| pubmed:affiliation |
Division of Genomic Medicine, University of Sheffield School of Medicine and Biomedical Sciences, Sheffield, United Kingdom. d.h.dockrell@sheffield.ac.uk
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|