Source:http://linkedlifedata.com/resource/pubmed/id/16849486
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2006-7-19
|
| pubmed:abstractText |
The fungus, Histoplasma capsulatum, produces a persistent infection. Reactivation histoplasmosis is largely a result of impaired immunity, but the perturbations associated with escape of the fungus from host defenses remain ill-defined. We analyzed a murine model of reactivation to elucidate the host defects that permit reactivation. C57BL/6 mice were infected intranasally and, 42 days later, they were depleted of CD4(+) and CD8(+) cells. Elimination of these cells, but not either alone, produced a persistent infection over several weeks. Neutralization of IFN-gamma, TNF-alpha, or both did not induce reactivation. Endogenous IL-10 exacerbated reactivation. Depletion of T cells in B cell(-/-) mice induced a markedly higher burden in organs when compared with wild type. However, the infection remained persistent. Elimination of CD4(+) cells alone or neutralization of cytokines increased the fungal load. The persistent infection was not dependent on gammadelta T cells or NK cells. Elimination of Thy-1.2(+) cells in mice given mAb to CD4 and CD8 transformed reactivation into a progressive, lethal infection in B cell(-/-) and wild-type mice, but the tempo of progression was accelerated in the former. The data reveal the complex control by the host to prevent reactivation of this fungus.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
177
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1763-71
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:16849486-Animals,
pubmed-meshheading:16849486-Antigens, CD4,
pubmed-meshheading:16849486-Antigens, CD8,
pubmed-meshheading:16849486-B-Lymphocytes,
pubmed-meshheading:16849486-Cytokines,
pubmed-meshheading:16849486-Histoplasma,
pubmed-meshheading:16849486-Histoplasmosis,
pubmed-meshheading:16849486-Lung,
pubmed-meshheading:16849486-Lymphocyte Depletion,
pubmed-meshheading:16849486-Mice,
pubmed-meshheading:16849486-Mice, Inbred C57BL,
pubmed-meshheading:16849486-Mice, Knockout,
pubmed-meshheading:16849486-Mice, Mutant Strains,
pubmed-meshheading:16849486-Mice, Nude,
pubmed-meshheading:16849486-Mice, Transgenic,
pubmed-meshheading:16849486-Nitric Oxide,
pubmed-meshheading:16849486-Recurrence,
pubmed-meshheading:16849486-Severity of Illness Index,
pubmed-meshheading:16849486-Spleen,
pubmed-meshheading:16849486-T-Lymphocyte Subsets
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
B cells and CD4-CD8- T cells are key regulators of the severity of reactivation histoplasmosis.
|
| pubmed:affiliation |
Division of Infectious Diseases, Veterans Affairs Hospital, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|