<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>The aim of this study was to investigate the effects of
elevated glucose concentrations on complement receptor–
and Fc<italic>γ</italic> receptor–mediated phagocytosis in normal human
neutrophils. D-Glucose at 15 or 25 mM dose-dependently
inhibited both complement receptor– and Fc<italic>γ</italic> receptor–
mediated phagocytosis, as compared to that at a normal
physiological glucose concentration. The protein kinase
C (PKC) inhibitors GF109203X and Go6976 both dose dependently
and completely reversed the inhibitory effect of
25 mM D-glucose on phagocytosis. Complement receptor–
mediated phagocytosis was dose-dependently inhibited by
the cell permeable diacylglycerol analogue 1,2-dioctanoyl<italic>sn</italic>-
glycerol (DAG), an effect that was abolished by PKC
inhibitors. Furthermore, suboptimal inhibitory concentrations
of DAG and glucose showed an additive inhibitory effect
on complement receptor–mediated phagocytosis. The
authors conclude that elevated glucose concentrations can
inhibit complement receptor and Fc<italic>γ</italic> receptor–mediated
phagocytosis in normal human neutrophils by activating
PKC<italic>α</italic> and/or PKC<italic>β</italic>, an effect possibly mediated by DAG.</p>
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Exp Diabesity Res. 2003; 4(2):125-132