Abstract
Lysophosphatidylcholine (LPC) accumulates in inflammatory tissues, where neutrophils are recruited to generate superoxide anions (O2.-). Here, we show that LPC stimulates O2.- generation in human neutrophils and that the activity is inhibited with phosphatidylinositol 3-kinase (PI3 kinase) inhibitors, but not with protein kinase C (PKC) inhibitors. Furthermore, we demonstrate that LPC activates PI3 kinase in neutrophils. Thus, LPC might contribute to host defense by generating O2.- in neutrophils through PI3 kinase activation, but not through PKC activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androstadienes / pharmacology
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Cell Survival
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Enzyme Activation
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Enzyme Inhibitors / pharmacology
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Humans
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In Vitro Techniques
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Kinetics
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Lysophosphatidylcholines / pharmacology*
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology
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Neutrophils / cytology
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Neutrophils / drug effects
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Neutrophils / physiology*
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Phosphatidylinositol 3-Kinases / blood*
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Phosphoinositide-3 Kinase Inhibitors
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / blood
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Superoxides / blood*
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Tetradecanoylphorbol Acetate / pharmacology
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Wortmannin
Substances
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Androstadienes
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Enzyme Inhibitors
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Lysophosphatidylcholines
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Phosphoinositide-3 Kinase Inhibitors
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Superoxides
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N-Formylmethionine Leucyl-Phenylalanine
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Protein Kinase C
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Tetradecanoylphorbol Acetate
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Wortmannin