Hyperglycemia-induced protein kinase C (PKC) activation inhibits phagocytosis of C3b- and IgG-opsonized yeast particles in normal human neutrophils
2003 (English)In: Experimental Diabesity Research, ISSN 1543-8600, E-ISSN 1543-8619, Vol. 4, no 2, 125-132 p.Article in journal (Refereed) Published
The aim of this study was to investigate the effects of elevated glucose concentrations on complement receptor- and Fcgamma receptor-mediated phagocytosis in normal human neutrophils. D-Glucose at 15 or 25 mM dose-dependently inhibited both complement receptor- and Fcgamma 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-sn-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 Fcgamma receptor-mediated phagocytosis in normal human neutrophils by activating PKCalpha and/or PKCbeta, an effect possibly mediated by DAG.
Place, publisher, year, edition, pages
2003. Vol. 4, no 2, 125-132 p.
IdentifiersURN: urn:nbn:se:umu:diva-4928DOI: 10.1155/EDR.2003.125PubMedID: 14630574OAI: oai:DiVA.org:umu-4928DiVA: diva2:144219