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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
38
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pubmed:dateCreated |
2003-9-15
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pubmed:abstractText |
Histoplasma capsulatum (Hc) is a facultative intracellular fungal pathogen that causes acute and chronic pneumonia. In this study, we investigated the role of the pulmonary collectins, surfactant proteins (SP) A and D, in the clearance of Hc yeast from the lung. Exposure of yeast to either collectin induced a dose-dependent decrease in [3H]leucine incorporation by several strains of Hc. This decrement was attributed to killing of the collectin-exposed yeast since it failed to grow on agar medium. Exposure to SP-A or -D resulted in increased yeast permeability based on a leak of protein from the organism and enhanced access of an impermeant substrate to intracellular alkaline phosphatase. Inbred and outbred SP-A null (-/-) mice were modestly more susceptible to pulmonary infection with Hc than strain and age-matched SP-A (+/+) control mice. The increase in susceptibility was associated with a decrement in the number of CD8+ cells in the lungs of SP-A-/- mice. Neither SP-A nor SP-D inhibited the growth of macrophage-internalized Hc. We conclude that the SP-A and SP-D are antimicrobial proteins that directly inhibit the growth of Hc by increasing permeability of the organism and that Hc gains asylum from collectin-mediated killing by rapid entry into pulmonary macrophages.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
278
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
36250-6
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12857753-Agar,
pubmed-meshheading:12857753-Alkaline Phosphatase,
pubmed-meshheading:12857753-Alleles,
pubmed-meshheading:12857753-Animals,
pubmed-meshheading:12857753-Cell Division,
pubmed-meshheading:12857753-Collectins,
pubmed-meshheading:12857753-Dose-Response Relationship, Drug,
pubmed-meshheading:12857753-Flow Cytometry,
pubmed-meshheading:12857753-Histoplasma,
pubmed-meshheading:12857753-Humans,
pubmed-meshheading:12857753-Leukocytes,
pubmed-meshheading:12857753-Lung,
pubmed-meshheading:12857753-Macrophages,
pubmed-meshheading:12857753-Mice,
pubmed-meshheading:12857753-Mice, Inbred C3H,
pubmed-meshheading:12857753-Mice, Transgenic,
pubmed-meshheading:12857753-Pulmonary Surfactant-Associated Protein A,
pubmed-meshheading:12857753-Pulmonary Surfactant-Associated Protein D,
pubmed-meshheading:12857753-Rats,
pubmed-meshheading:12857753-Rats, Sprague-Dawley,
pubmed-meshheading:12857753-Recombinant Proteins,
pubmed-meshheading:12857753-Spleen,
pubmed-meshheading:12857753-Stem Cells,
pubmed-meshheading:12857753-Time Factors
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pubmed:year |
2003
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pubmed:articleTitle |
Macrophage-independent fungicidal action of the pulmonary collectins.
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pubmed:affiliation |
Veterans Affairs Medical Center, Cincinnati, Ohio 45220, USA. frank.mccormack@uc.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
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