Abstract.
Objective: This study investigated the effects of insulin on the phagocytosis of C3bi – and IgG-opsonized yeast particles in normal human neutrophils.
Methods: Neutrophils were incubated in different insulin concentrations for 30 minutes and stimulated by C3bi – or IgG-opsonized yeast particles. Phagocytosis was quantified by both light microscopy and FACscan flow cytometry. Laser confocal microscopy was used for quantification of F-actin levels.
Results: Elevated insulin concentrations decreased neutrophil phagocytosis of both types of targets. This defect was shown to be in part due to a delayed phagocytosis in the presence of insulin. Following a 30 minute incubation, insulin was found to increase the accumulation of cortical F-actin, without affecting the total cellular F-actin content. The specific PKCα/β inhibitor, Go6976, abolished the insulin-mediated increase in cortical F-actin content and both Go6976 and the PKCα/β/δ/ε-specific inhibitor GF109203X reversed the inhibitory effects of insulin on phagocytosis.
Conclusion: Hyperinsulinemia in vitro can inhibit phagocytosis of opsonized targets in normal human neutrophils. This effect of insulin is dependent on activation of PKCα and/or PKCβ, and these insulin signals may interfere with the dynamic assembly/disassembly and/or distribution of F-actin, which is required for the phagocytosis process.
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Received 8 July 2005; accepted 13 October 2005 without revision I. Ahnfelt-Rønne
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Saiepour, D., Sehlin, J. & Oldenborg, P.A. Insulin inhibits phagocytosis in normal human neutrophils via PKCα/β-dependent priming of F-actin assembly. Inflamm. res. 55, 85–91 (2006). https://doi.org/10.1007/s00011-005-0009-1
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DOI: https://doi.org/10.1007/s00011-005-0009-1