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Acute Regulation of Glucose Transport After Activation of Human
Peripheral Blood Neutrophils by Phorbol Myristate Acetate,
fMLP, and Granulocyte-Macrophage Colony-Stimulating Factor
An S. Tan,
Nuzhat Ahmed, and
Michael V. Berridge
From the Malaghan Institute of Medical Research, Wellington School of
Medicine, Wellington South, New Zealand.
Activation of human peripheral blood neutrophils by pathogens or by
phorbol myristate acetate (PMA), fMLP, or myeloid growth factors
generates a respiratory burst in which superoxide production plays an
important role in killing invading microorganisms. Although the
increased energy demands of activated neutrophils would be expected to
be associated with increased glucose uptake and utilization, previous
studies have shown that PMA inhibits 2-deoxyglucose (2-DOG) uptake. In
this study, we show that PMA activation of neutrophils, isolated by
methods not involving hypotonic lysis, increases the rate of 2-DOG
uptake and results in a 1.6-fold to 2.1-fold increase in transporter
affinity for glucose without changing Vmax. Increased transporter affinity in response to PMA was also observed with 3-O-methyglucose, which is not phosphorylated, and inclusion of glucose
in the activation medium further increased respiratory burst activity.
Increased 2-DOG uptake and increased transporter affinity for glucose
were also observed with the peptide activator, fMLP, and with
granulocyte-macrophage colony-stimulating factor (GM-CSF). The protein
kinase C (PKC) inhibitor, calphostin C, and the tyrosine kinase
inhibitor, genistein, inhibited both PMA- and fMLP-stimulated 2-DOG
uptake. In contrast, genistein inhibited fMLP-induced superoxide
production, but had little effect on the PMA-induced response, while
staurosporine differentially inhibited PMA-induced superoxide
production. These results show that neutrophil activation involves
increased glucose transport and intrinsic activation of glucose
transporter molecules. Both tyrosine kinases and PKC are implicated in
the activation process.
Blood, Vol. 91 No. 2 (January 15), 1998:
pp. 649-655
© 1998 by The American Society of Hematology.
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