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Reticuloendothelial blockade: effect of puromycin on opsonin-dependent recovery
Science (New York, N.Y.)
|November 1, 1968
Abstract:
Reticuloendothelial blockade induced by the administration of a gelatinized "reticuloendothelial test lipid emulsion" is due to a loss of opsonic activity in the plasma. Recovery from blockade, which is associated with restoration of plasma opsonins, was inhibited by the administration of puromycin. The effect of puromycin appears to be mediated by inhibition of opsonin formation rather than a puromycin-induced macrophage defect in phagocytosis.
Insights
Reticuloendothelial blockade, caused by lipid emulsion, results from reduced plasma opsonins. Puromycin inhibits recovery by blocking opsonin formation, not macrophage function.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Reticuloendothelial blockade is induced by lipid emulsions, leading to decreased plasma opsonic activity.
- Recovery from blockade involves the restoration of plasma opsonins.
Purpose of the Study:
- To investigate the mechanism by which puromycin inhibits recovery from reticuloendothelial blockade.
- To determine if puromycin affects opsonin formation or macrophage phagocytic capacity.
Main Methods:
- Induction of reticuloendothelial blockade using a gelatinized lipid emulsion in a model system.
- Administration of puromycin to assess its effect on recovery from blockade.
- Measurement of plasma opsonic activity and macrophage phagocytosis.
Main Results:
- Puromycin administration inhibited the recovery from reticuloendothelial blockade.
- The inhibitory effect of puromycin was associated with suppressed opsonin formation.
- Puromycin did not appear to induce a macrophage defect in phagocytosis.
Conclusions:
- Puromycin's inhibition of reticuloendothelial blockade recovery is primarily due to the suppression of opsonin synthesis.
- The findings suggest that opsonin production is crucial for restoring reticuloendothelial function after blockade.