Effect of Phorbol Myristate Acetate on the Oxidative Metabolism of Human Polymorphonuclear Leukocytes

The addition of 0.1 µg/ml of phorbol myristate acetate (PMA) to a suspension of resting human neutrophils causes a marked stimulation of all aspects of cellular oxidative metabolism normally associated with phagocytosis. PMA induces a greatly increased rate of glucose oxidation via the hexose monoph...

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Bibliographic Details
Published in:Blood 1976-04, Vol.47 (4), p.545-554
Main Authors: DeChatelet, Lawrence R., Shirley, Pamela S., Johnston, Richard B.
Format: Article
Language:English
Subjects:
Amino Acids - metabolism
Deoxyglucose - metabolism
Glucose - metabolism
Humans
Luminescent Measurements
Neutrophils - metabolism
Phagocytosis
Phorbols - pharmacology
Tetradecanoylphorbol Acetate - pharmacology
Time Factors
Zymosan - metabolism
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Summary:The addition of 0.1 µg/ml of phorbol myristate acetate (PMA) to a suspension of resting human neutrophils causes a marked stimulation of all aspects of cellular oxidative metabolism normally associated with phagocytosis. PMA induces a greatly increased rate of glucose oxidation via the hexose monophosphate shunt, increased production of superoxide anion and of hydrogen peroxide, increased cellular chemiluminescence, and increased iodination of protein material. The time course of hexose monophosphate shunt activation and of chemiluminescence are similar to those observed following phagocytosis of opsonized zymosan; the levels of activation achieved in all cases approximate those seen following phagocytosis. These phenomena are not simply reflections of altered cellular permeability, since PMA actually inhibits the uptake of radioactive 2-deoxyglucose and of uniformly labeled amino acids. The addition of PMA similarly inhibits the uptake of 14C-labeled bacteria, suggesting a competition between the effect of the chemical and the process of phagocytosis. These results suggest that PMA activates the cell in the same manner as does phagocytosis. This compound should provide a useful tool for elucidating the metabolic events underlying the phenomena of phagocytosis and bacterial killing by polymorphonuclear leukocytes.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V47.4.545.545