• Kwok-Tung Lu, Yi-Wen Wang, Jen-Tsung Yang, Yi-Ling Yang, and Hsing-I Chen.
• Department of Life Science, National Taiwan Normal University, Taipei, Taiwan.
• J. Neurotrauma. 2005 Aug 1;22(8):885-95.

AbstractInterleukin-1 (IL-1) has many roles in the brain in addition to mediating inflammatory processes in the glia, and has also been implicated in neurodegenerative disease. Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity and mortality in young persons. We conducted a study to assess the effect of IL-1 on the TBI-induced death of hippocampal neurons. After TBI was induced in adult male Sprague-Dawley rats under anesthesia, we evaluated neuronal damage score through microscopic examination and Pulsinelli's grading system. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to measure the levels of IL-1alpha and IL- 1beta in brain tissue at different points after the induction of TBI. Over a 4-day period, the specific sites of release of IL-1alpha and IL-1beta in the brain were elucidated by immunocytochemistry with double- labeling. TBI to the hippocampus was followed by disruption of the blood-brain barrier and severe neuronal loss. Levels of IL-1alpha RNA and protein were significantly elevated at 3 h after TBI, peaked at 12 h, and remained elevated for 168 h. IL-1beta RNA and protein expression were also elevated at 3 h after TBI, but remained so only for 48 h. Our findings indicate that the observed TBI-induced increases in IL-1alpha and IL-1beta occur largely through release of these cytokines from neurons and astrocytes, respectively. Intraventricular administration of antibodies to IL-1alpha and IL-1beta before TBI significantly attenuated the TBI-induced loss of hippocampal neurons. These results show that IL-1alpha and IL-1beta play important roles in the TBI-induced loss of hippocampal neurons.

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