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Abstract #18532 Published in IGR 3-3
Increased post-traumatic survival of neurons in IL-6-knockout mice on a background of EAE susceptibility
Fisher J; Mizrahi T; Schori H; Yoles E; Levkovitch-Verbin H; Haggiag S; Revel M; Schwartz MJournal of Neuroimmunology 2001; 119: 1-9
Axonal injury initiates a process of neuronal degeneration, with resulting death of neuronal cell bodies. The authors show that in C57BL/ 6J mice, previously shown to have a limited ability to manifest a post-traumatic protective immunity, the rate of neuronal survival is increased if IL-6 is deficient during the first 24 hours after optic nerve injury. Immunocytochemical staining preformed seven days after the injury revealed an increased number of activated microglia in the IL-6-deficient mice compared to the wild-type mice. In addition, IL- 6-deficient mice showed an increased resistance to glutamate toxicity. These findings suggest that the presence of IL-6 during the early post-traumatic phase, at least in mice that are susceptible to autoimmune disease development, has a negative effect on neuronal survival. This further substantiates the contention that whether immune-derived factors are beneficial or harmful for nerve recovery after injury depends on the phenotype of the immune cells and the timing and nature of their dialogue with the damaged neural tissue.
Dr J. Fisher, Department of Neurobiology, The Weizmann Institute of Science, 76100, Rehovot, Israel
Classification:
1.3 Pathogenesis (Part of: 1 General aspects)