Endogenous Interleukin-17a Contributes to Normal Spatial Memory Retention but Does Not Affect Early Behavioral or...

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 mice in beam balance, Morris water maze performance, or lesion volume after CCI. Surprisingly, naïve il17a ^-/- mice performed significantly (p = 0.02) worse than naïve 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 naïve mice.