Insulin inhibits phagocytosis in normal human neutrophils via PKCα/β-dependent priming of F-actin assembly |
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Authors: | D Saiepour J Sehlin P -A Oldenborg |
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Institution: | 1. Department of Integrative Medical Biology, Section for Histology and Cell Biology, Ume? University, 901 87, Ume?, Sweden
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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.
Received 8 July 2005; accepted 13 October 2005 without revision I. Ahnfelt-R?nne |
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Keywords: | Polymorphonuclear leukocytes Diabetes Phagocytosis PKC Insulin F-actin Complement receptors Fcγ receptors |
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