Hyperglycemia-Induced Protein Kinase C Activation Inhibits Phagocytosis of C3b- and Immunoglobulin G–Opsonized Yeast Particles in Normal Human Neutrophils |
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Authors: | Daniel Saiepour Janove Sehlin Per-Arne Oldenborg |
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Institution: | 1. Department of Integrative Medical Biology, Section for Histology and Cell Biology, Umeå University, Umeå, SE-901 87, Sweden, |
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Abstract: | The aim of this study was to investigate the effects of
elevated glucose concentrations on complement receptor–
and Fcγ receptor–mediated phagocytosis in normal human
neutrophils. D-Glucose at 15 or 25 mM dose-dependently
inhibited both complement receptor– and Fcγ 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-dioctanoylsn-
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 Fcγ receptor–mediated
phagocytosis in normal human neutrophils by activating
PKCα and/or PKCβ, an effect possibly mediated by DAG. |
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