Endogenous Interleukin-17a Contributes to Normal Spatial Memory Retention but Does Not Affect Early Behavioral or Neuropathological Outcomes after Experimental Traumatic Brain Injury

Interleukin-17 (IL-17) is a proinflammatory cytokine primarily secreted in the brain by inflammatory T lymphocytes and glial cells. IL-17(+) T-helper (Th17) cells are increased in the ipsilateral hemisphere after experimental traumatic brain injury (TBI), and IL-17 levels are increased in serum and brain tissue. We hypothesized that il17a and related gene expression would be increased in brain tissue after TBI in mice and il17a(-/-) mice would demonstrate neuroprotection versus wild type. The controlled cortical impact (CCI) model of TBI in adult male C57BL6/J mice was used for all experiments. Data were analyzed by analysis of variance (ANOVA) or repeated-measures two-way ANOVA with the Bonferroni correction. A value of p < 0.05 determined significance. Expression of il17a was significantly reduced in the ipsilateral cortex and hippocampus by day 3 after TBI, and expression remained low at 28 days. There were no differences between il17a(-/-) and il17a(+/+) mice in beam balance, Morris water maze performance, or lesion volume after CCI. Surprisingly, naive il17a(-/-) mice performed significantly (p = 0.02) worse than naive il17a(+/+) mice on the probe trial. In conclusion, sustained depression of il17a gene expression was observed in brains after TBI in adult mice. Genetic knockout of IL-17 was not neuroprotective after TBI. IL-17a may be important for memory retention in naive mice.