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1571: ROLE OF IL-17 AFTER TRAUMATIC BRAIN INJURY IN ADULT MICE

www.ccmjournal.org Critical Care Medicine • Volume 46 • Number 1 (Supplement) Learning Objectives: Neuroinflammation after traumatic brain injury may lead to secondary brain injury and worse neurologic outcomes. The cytokine IL-17, produced largely by T-cells expressing the transcription factor RORt (rorc gene), has been associated with harmful inflammation in stroke and multiple sclerosis. We hypothesized that il17 expression would be elevated after TBI in mice and cause worse neurologic outcome. Methods: Traumatic brain injury was performed in adult male C57BL6/J mice using the controlled cortical impact (CCI) model with velocity 5 m/s, depth 1.2mm. Mice (5–6/group) were sacrificed at 1, 3, 7, 14, and 28 days after injury and RNA extracted from brain tissue for gene expression analysis. IL-17(-/-) and IL-17(+/+) C57BL6/J mice (9 10/group) underwent more severe CCI (6 m/s, depth 1.8mm) and behavioral testing was performed. Naïve mice served as controls. Data were analyzed by ordinary two-way ANOVA or rmANOVA with Bonferonni’s correction and p < 0.05 as significant. Results: No significant change was seen in il17 expression in the ipsilateral cortex or hippocampus after TBI. We observed a significant decrease in rorc expression in the cortex and significant increase expression in the hippocampus by 72 hours that was still observed at 28 days post-injury (p < 0.05). There were no differences between wild-type and il17 knockout mice in beam-balance or Morris water maze performance after CCI. Naïve IL-17(-/-) mice performed significantly worse than wild-type mice on probe trial, suggesting impaired memory retention. Conclusions: Il17 gene expression was not significantly altered after TBI in adult mice. IL-17(-/-) mice did not perform better in Morris water maze after injury. IL-17 may be important for memory retention in uninjured mice.