Increased post-traumatic survival of neurons in IL-6-knockout mice on a background of EAE susceptibility

Axonal injury initiates a process of neuronal degeneration, with resulting death of neuronal cell bodies. We show here that in C57BL/6J mice, previous ly 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 d uring the first 24 hours after optic nerve injury. Immunocytochemical stain ing preformed 7 days after the injury revealed an increased number of activ ated microglia in the IL-6-deficient mice compared to the wild-type mice. I n addition, IL-6-deficient mice showed an increased resistance to glutamate toxicity. These findings suggest that the presence of IL-6 during the earl y post-traumatic phase, at least in mice that are susceptible to autoimmune disease development, has a negative effect on neuronal survival. This furt her substantiates the contention that whether immune-derived factors are be neficial or harmful for nerve recovery after injury depends on the phenotyp e of the immune cells and the timing and nature of their dialog with the da maged neural tissue. (C) 2001 Elsevier Science B.V. All rights reserved.