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Suppression of polymorphonuclear leukocyte bactericidal activity by suramin
E Roilides1, P Paschalides, A Freifeld
1Infectious Diseases Section, National Cancer Institute, Bethesda, Maryland 20892.
Antimicrobial Agents and Chemotherapy
|March 1, 1993
Summary
Suramin impairs polymorphonuclear leukocyte (PMN) bactericidal activity against Staphylococcus aureus, but not fungal activity. Granulocyte colony-stimulating factor may mitigate this defect, suggesting potential implications for infection susceptibility.
Area of Science:
- Immunology
- Pharmacology
Background:
- Polyanionic compounds like suramin possess antineoplastic properties.
- Polymorphonuclear leukocytes (PMNs) are critical for combating bacterial and fungal infections.
Purpose of the Study:
- To investigate the in vitro effects of suramin on key polymorphonuclear leukocyte (PMN) functions.
- To assess suramin's impact on PMN fungicidal and bactericidal activities, as well as phagocytosis and superoxide production.
Main Methods:
- PMNs from healthy donors were incubated with varying concentrations of suramin (1-1,000 µg/ml).
- Functional parameters including viability, chemotaxis, phagocytosis, superoxide production, and antimicrobial activity were assessed.
- Effects of human serum and granulocyte colony-stimulating factor (G-CSF) were also evaluated.
Main Results:
- Suramin did not affect PMN viability, chemotaxis, or superoxide production.
- Fungicidal activity against Candida albicans was largely unaffected, with slight suppression at high concentrations (>500 µg/ml).
- Bactericidal activity against Staphylococcus aureus was significantly suppressed at concentrations ≥100 µg/ml, and phagocytosis was impaired at ≥10 µg/ml.
Conclusions:
- Suramin impairs PMN bactericidal function and phagocytosis of Staphylococcus aureus, but not fungicidal activity against Candida albicans.
- The presence of serum did not prevent suramin's inhibitory effect on bactericidal activity.
- Granulocyte colony-stimulating factor (G-CSF) treatment partially restored the bactericidal defect, suggesting a potential therapeutic strategy to counteract suramin-induced immunosuppression.