Lipopolysaccharide and hypoxia/ischemia induced IL-2 expression by microglia in neonatal brain

Neuroreport. 2008 Jul 2;19(10):997-1002. doi: 10.1097/WNR.0b013e3283036e88.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Brain / pathology*
  • Calcium-Binding Proteins / genetics
  • Calcium-Binding Proteins / metabolism
  • Cells, Cultured
  • Enzyme-Linked Immunosorbent Assay / methods
  • Female
  • Gene Expression Regulation / drug effects
  • Hypoxia / pathology*
  • Interleukin-2 / genetics
  • Interleukin-2 / metabolism*
  • Lipopolysaccharides / pharmacology*
  • Male
  • Microfilament Proteins
  • Microglia / drug effects*
  • Microglia / metabolism*
  • Pregnancy
  • RNA, Messenger / metabolism
  • Random Allocation
  • Rats
  • Rats, Inbred Lew
  • Receptors, Interleukin-2 / genetics
  • Receptors, Interleukin-2 / metabolism
  • Time Factors


  • Aif1 protein, rat
  • Calcium-Binding Proteins
  • Interleukin-2
  • Lipopolysaccharides
  • Microfilament Proteins
  • RNA, Messenger
  • Receptors, Interleukin-2