Transient ischemia-induced changes of interleukin-2 and its receptor beta immunoreactivity and levels in the gerbil hippocampal CA1 region

Brain Res. 2006 Aug 23;1106(1):197-204. doi: 10.1016/j.brainres.2006.05.098. Epub 2006 Jul 11.

Abstract

Interlukin-2 (IL-2) is an important cytokine in the brain: IL-2 and its receptors are involved with inflammatory processes. Chronological changes in IL-2 level in serum, and IL-2 and its receptor (IL-2 receptor beta, IL-2Rbeta) immunoreactivities and levels were examined in the hippocampal CA1 region after transient forebrain ischemia in gerbils. IL-2 level in serum significantly decreased 12 h after ischemia/reperfusion. IL-2 immunoreactivity was detected in the somata of pyramidal cells in sham-operated group. At 15 min after ischemia, IL-2 immunoreactivity was shown in non-pyramidal cells as well as pyramidal cells. One day after ischemia, IL-2 immunoreactivity was lowest, and IL-2 immunoreactivity is shown in non-pyramidal cells from 2 days after ischemia. Four days after ischemia, IL-2 immunoreactivity was shown in dying pyramidal cells. IL-2Rbeta immunoreactivity in the sham-operated and 15 min-3 min post-ischemic groups is detected in the cell membrane of pyramidal cells. From 3 h after ischemia, IL-2Rbeta immunoreactivity is found in cytoplasm and nuclei, but not in cell membrane. IL-2Rbeta immunoreactivity decreases from 6 h after ischemia and is shown mainly in non-pyramidal cells from 3 days after ischemia. The data of Western blot analyses for IL-2 and IL-2Rbeta was similar to the immunohistochemical data. IL-2 infusion into cerebrospinal fluid did not protect hippocampal neurons from ischemic damage. These results suggest that IL-2 and IL-2Rbeta show malfunction from 3 h after ischemia, and exogenous IL-2 does not protect ischemic neuronal damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Infarction / immunology
  • Brain Infarction / metabolism
  • Brain Infarction / physiopathology
  • Brain Ischemia / immunology*
  • Brain Ischemia / metabolism
  • Brain Ischemia / physiopathology
  • Cell Death / drug effects
  • Cell Death / immunology
  • Disease Models, Animal
  • Down-Regulation / immunology
  • Encephalitis / immunology
  • Encephalitis / metabolism
  • Encephalitis / physiopathology
  • Gerbillinae
  • Hippocampus / immunology*
  • Hippocampus / metabolism
  • Hippocampus / physiopathology
  • Immunohistochemistry
  • Injections, Intraventricular
  • Interleukin-2 / immunology*
  • Interleukin-2 / metabolism
  • Interleukin-2 / pharmacology
  • Ischemic Attack, Transient / immunology*
  • Ischemic Attack, Transient / metabolism
  • Ischemic Attack, Transient / physiopathology
  • Male
  • Nerve Degeneration / immunology
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / physiopathology
  • Neuroprotective Agents / immunology
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / pharmacology
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / immunology
  • Pyramidal Cells / metabolism
  • Receptors, Interleukin-2 / agonists
  • Receptors, Interleukin-2 / immunology*
  • Receptors, Interleukin-2 / metabolism
  • Time Factors
  • Treatment Failure

Substances

  • Interleukin-2
  • Neuroprotective Agents
  • Receptors, Interleukin-2