Fig. 8

IL-10 promotes an anti-inflammatory environment in cortex of NOX2^−/− TBI mice. (a) Neutralizing anti-IL-10 (αIL-10; 1 mg/ml, i.c.v.) or control αIgG2b K was administered to WT or NOX2^−/− TBI mice for 72 h, and ipsilateral cortex tissue was collected for mRNA analysis. (b-f) TBI increased IL-4Rα (b), SOCS3 (c), TGFβ (d), YM1 (e), and Arg1 (f) mRNA expression in the ipsilateral cortex of WT and NOX2^−/−mice (^*** P < 0.001, vs. sham; ANOVA). TBI effect on anti-inflammatory marker expression was significantly increased in NOX2^−/− TBI mice when compared to WT TBI mice (⁺ P < 0.05, ⁺⁺ P < 0.01, ⁺⁺⁺ P < 0.001, WT αIgG2b K TBI vs. NOX2^−/− αIgG2b K TBI; ANOVA). αIL-10 treatment significantly reduced the expression of all anti-inflammatory markers in NOX2^−/− TBI mice (^# P < 0.05, ^## P < 0.01, NOX2^−/− αIgG2b K TBI vs. NOX2^−/− αIL-10 TBI; ANOVA). All data are expressed as means (±SEM; n = 6)