IL6 Deficiency Affects Function After Traumatic Brain Injury

ObjectiveInterleukin-6 (IL6) is a major inflammatory mediator and one of the first cytokines produced after traumatic brain injury (TBI). This study evaluates early behavioral changes and acute inflammation after TBI in IL6 knock-out mice using electromagnetic controlled cortical impact.MethodsIL6 knock-out (KO) and C57BL/6 (WT) male mice were subjected to TBI or sham injury (n = 6 mice per group) using electromagnetic controlled cortical impact. Behavioral deficits were tested by standard performance tests. Brain IL1β expression was measured by ELISA and HSP70 expression was measured by Western blot.ResultsAfter TBI, KO showed reduced performance on the neuroscreen compared with wild type (KO 3.2 ± 0.7 versus WT 4.7 ± 0.2 points, P = 0.007), less exploratory activity in the open field test (KO 1090.2 ± 1799.2 versus WT 5636.8 ± 1291.8 regions explored per hour, P = 0.003) less rearing behavior in the open field test (KO 36.4 ± 79.2 versus WT 346.5 ± 18.5 rearing per hour, P = 0.0006), reduced travel on the rotarod (KO 3.5 ± 4.0 versus WT 13.0 ± 4.0 cm, P = 0.0109), and reduced time balanced on the rotarod (KO 15.0 ± 11.5 versus WT 36.2 ± 5.9 s, P = 0.0109). After TBI, IL6 knock-out mice had significantly elevated IL1β (KO 58.16 ± 17.54 versus WT 14.98 ± 8.33 pg/mL, P = 0.003 and nonsignificantly increased HSP70 levels (KO 0.93 ± 0.96 versus WT 0.68 ± 0.97, P = 0.77).ConclusionIL6 deficiency after TBI is associated with poor behavior performance, and appears to affect expression of IL1β and, possibly, HSP70.