Development of Macrophage Anticryptococcal Activityin VitroIs Dependent on Endogenous M-CSF
Autor: | Gary L. Gilmore, David A. Stevens, Richard K. Shadduck, Elmer Brummer |
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Rok vydání: | 1998 |
Předmět: |
Male
Serial dilution medicine.drug_class Immunology Receptor Macrophage Colony-Stimulating Factor Stimulation Endogeny Monoclonal antibody Mice medicine Animals Macrophage Receptor Mice Inbred BALB C biology Mouse strain Macrophage Colony-Stimulating Factor Macrophages Antibodies Monoclonal Macrophage Activation Molecular biology Rats Cryptococcus neoformans biology.protein Rabbits Antibody |
Zdroj: | Cellular Immunology. 189:144-148 |
ISSN: | 0008-8749 |
DOI: | 10.1006/cimm.1998.1366 |
Popis: | We previously showed that nonactivated resident murine peritoneal macrophages (PM) from five strains (e.g., BALB/c) have C′-dependent fungistasis forCryptococcus neoformansin 24-h coculture, but not CD-1 PM unless culture time was extended or M-CSF treatment was used. We studied effect of a rat IgG1monoclonal (m) antibody (Ab) to murine M-CSF receptor on this anticryptococal activity. Culture of BALB/c PM with mAb, diluted 1:10, prechallenge reduced fungistasis from 58 to 21% (P< 0.01), whereas further 10-fold dilutions did not. Moreover, M-CSF pretreatment (5000 U/ml) significantly enhanced fungistasis (to 85%), whereas adding mAb 1:10 or 1:100 reduced that (to 58 and 77%, respectively,P< 0.01). In 48-h culture CD-1 PM had 39% fungistasis, reduced to 0% by mAb, M-CSF treatment of CD-1 PM increased fungistasis to 72%, which was reduced to 13 or 58% (P< 0.001) by 1:10 or 1:100 mAb, respectively. Complete blocking by mAb of CD-1 PM activity was consistent with lack of measurable early endogenous CD-1 M-CSF production. Increasing exogenous M-CSF could overcome the inhibition by mAb (64% fungistasis BALB/c PM reduced to 11% with inhibition by mAb or increased to 94% with 5000 U/ml M-CSF; 37% with both mAb and M-CSF, 51% with mAb and 10,000 U/ml;P< 0.05, 5000 U/ml + mAb vs 10,000 U/ml + mAb). Moreover, rabbit Ab to M-CSF significantly reduced anticryptococcal activity of untreated BALB/c macrophages. In summary, development of PM fugistatic activity is dependent on endogenous M-CSF, since it is blocked by anti-receptor mAb (as is exogenous M-CSF stimulation) or anti-M-CSF Ab, and macrophages of the mouse strain with delayed activity had no measurable early M-CSF production. |
Databáze: | OpenAIRE |
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