Abstract
We have studied the interactions between activated microglia and injured motor neurons using an immortalized murine microglial cell line (BV-2) stimulated with either lipopolysaccharide (LPS) (Escherichia coli) or supernatant from serum-deprived motor neurons (NSC-34 cell line). Both stimuli induced BV-2 activation. Although both BV-2 supernatants induced a subsequent increase in NO generation in otherwise healthy NSC-34 cells, only LPS-activated microglial supernatant induced NSC-34 cell death through a TNF-alpha-dependent pathway. However, we observed a 20-fold increase in the amount of TNF-alpha required to kill NSC-34 cells in the absence of LPS-activated BV-2 cell supernatant, indicating that microglia secrete factor(s) that facilitate TNF-alpha-mediated motor neuron death in vitro.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyotrophic Lateral Sclerosis / immunology
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Amyotrophic Lateral Sclerosis / metabolism
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Amyotrophic Lateral Sclerosis / physiopathology
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Animals
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Antibodies / pharmacology
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Cell Communication / immunology*
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Cell Death / immunology*
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Cell Line, Transformed
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Cell Movement / drug effects
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Cell Movement / immunology
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Cell Survival / drug effects
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Cell Survival / immunology
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Central Nervous System / immunology*
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Central Nervous System / metabolism
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Central Nervous System / physiopathology
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Culture Media, Conditioned / pharmacology
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Culture Media, Serum-Free / pharmacology
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Gliosis / immunology*
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Gliosis / metabolism
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Gliosis / physiopathology
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Lipopolysaccharides / pharmacology
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Mice
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Microglia / immunology*
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Microglia / metabolism
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Motor Neurons / immunology*
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Motor Neurons / metabolism
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Motor Neurons / pathology
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Nitric Oxide / biosynthesis
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Nitric Oxide Synthase / metabolism
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Phagocytosis / drug effects
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Phagocytosis / immunology
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Tumor Necrosis Factor-alpha / immunology*
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Tumor Necrosis Factor-alpha / metabolism
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Antibodies
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Culture Media, Conditioned
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Culture Media, Serum-Free
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Lipopolysaccharides
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Tumor Necrosis Factor-alpha
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Nitric Oxide
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Nitric Oxide Synthase