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J. Biol. Chem., Vol. 278, Issue 51, 51075-51084, December 19, 2003

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Analysis of Interleukin-1-induced Cell Signaling Activation in Rat Hippocampus following Exposure to Gamma Irradiation

PROTECTIVE EFFECT OF EICOSAPENTAENOIC ACID^*

Aileen M. Lynch, Michelle Moore, Sarah Craig, Peter E. Lonergan, Darren S. Martin, and Marina A. Lynch

From the Department of Physiology, Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland

Among the many reported effects of irradiation in cells is activation of the stress-activated protein kinase, c-Jun N-terminal kinase (JNK), which has been shown to result in apoptotic cell death. The trigger that leads to JNK activation has not been identified, although, in rat hippocampus at least, irradiation-induced apoptosis has been coupled with increased accumulation of reactive oxygen species (ROS). Significantly, irradiation-induced changes in hippocampus are abrogated by treatment of rats with the polyunsaturated fatty acid, eicosapentaenoic acid (EPA). A close coupling between ROS accumulation and concentration of the pro-inflammatory cytokine, interleukin-1 (IL-1) in hippocampus has been reported, and the evidence suggests that IL-1 may be responsible for the enhanced ROS production. Here we set out to assess the possibility that whole body -irradiation increases IL-1 concentration in hippocampus and to investigate the consequences of such a change. We present evidence that reveals that the irradiation-induced increase in IL-1 concentration in hippocampus is accompanied by increased expression of IL-1 type I receptor and IL-1 accessory protein and increased activation of IL-1 receptor-activated kinase. These changes, which were coupled with increased activation of JNK and evidence of apoptotic cell death, were absent in hippocampus of rats that received EPA treatment. Significantly, EPA treatment enhanced hippocampal IL-10 concentration that was inversely correlated with IL-1 concentration. The data are consistent with the idea that EPA exerts anti-inflammatory and neuroprotective effects in the central nervous system.

Received for publication, July 22, 2003 , and in revised form, September 10, 2003.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 353-1608-1019; Fax: 353-1679-3545; E-mail: amlynch{at}tcd.ie.

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