Abstract
Delayed neuronal death associated with stroke has been increasingly linked to the immune response to the injury. Splenectomy prior to middle cerebral artery occlusion (MCAO) is neuroprotective and significantly reduces neuroinflammation. The present study investigated whether splenic signaling occurs through interferon gamma (IFNγ). IFNγ was elevated early in spleens but later in the brains of rats following MCAO. Splenectomy decreased the amount of IFNγ in the infarct post-MCAO. Systemic administration of recombinant IFNγ abolished the protective effects of splenectomy with a concurrent increase in INFγ expression in the brain. These results suggest a role for spleen-derived IFNγ in stroke pathology.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Brain Ischemia / pathology
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Brain Ischemia / physiopathology
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Cell Hypoxia
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Cells, Cultured
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Female
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Fluoresceins
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Fluorescent Dyes
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Immunohistochemistry
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Infarction, Middle Cerebral Artery / pathology
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Interferon-gamma / pharmacology
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Interferon-gamma / physiology*
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Laser-Doppler Flowmetry
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Ligation
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Male
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Middle Cerebral Artery / physiology
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Nerve Degeneration / physiopathology*
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Neuroglia / metabolism
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Neurons / drug effects
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Neurons / metabolism
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Oligodendroglia / metabolism
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Organic Chemicals
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Pregnancy
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Rats
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Rats, Sprague-Dawley
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Recombinant Proteins / pharmacology
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Signal Transduction / physiology
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Spleen / metabolism
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Spleen / physiopathology*
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Splenectomy
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Stroke / physiopathology*
Substances
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Fluoresceins
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Fluorescent Dyes
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Organic Chemicals
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Recombinant Proteins
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fluoro jade
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Interferon-gamma