Abstract
Using a model of perinatal brain lesions induced by lipopolysaccharide and hypoxia/ischemia, we hypothesized that interleukin-2 (IL-2), a neurotoxic cytokine, was enhanced within injured brains. We showed that lipopolysaccharide and hypoxia/ischemia enhanced both intracerebral IL-2 mRNA and protein levels, with a maximum increase upon lipopolysaccharide and hypoxia/ischemia. The lack of detectable T lymphocytes suggested the synthesis of IL-2 by neural cells. Lipopolysaccharide and hypoxia triggered IL-2 synthesis by cultured microglia with a peak after exposure to lipopolysaccharide and hypoxia. Double-labeling showed, in vivo and in vitro, that IL-2 immunoreactivity was colocalized with a microglia/macrophage marker. These results disclosed the ability of microglia to produce IL-2 and also suggest the implication of IL-2 in neural cell death triggered by perinatal lipopolysaccharide and hypoxia/ischemia exposures.
Original language | English (US) |
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Pages (from-to) | 997-1002 |
Number of pages | 6 |
Journal | NeuroReport |
Volume | 19 |
Issue number | 10 |
DOIs | |
State | Published - Jul 2 2008 |
Keywords
- Cerebral palsy
- Hypoxia/ischemia
- Interleukin-2
- Lipopolysaccharide
- Perinatal brain
ASJC Scopus subject areas
- General Neuroscience