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. 2020 Mar 11;40(11):2357–2370. doi: 10.1523/JNEUROSCI.2516-19.2020

Figure 4.

Figure 4.

IFN-β deficiency alters the inflammatory response after TBI. Cortical mRNA expression of Arg1, YM1, IL-10, SOCS3, and TGFβ was assessed in WT and IFN-β−/− sham and TBI mice. TBI significantly increased cortical mRNA expression of Arg1 (p = 0.0002; A), YM1 (p < 0.0001; B), IL-10 (p < 0.0001; C), TGFβ (p < 0.0001; D), and SOCS3 (p < 0.0001; E) in WT and IFN-β−/− mice. The effect of TBI on YM1 (p = 0.0022, WT TBI vs IFN-β−/− TBI) and IL-10 (p < 0.0001, WT TBI vs IFN-β−/− TBI) was significantly reduced in IFN-β−/− TBI mice compared with WT TBI mice. Hippocampal mRNA expression of Arg1, YM1, SOCS3, and TGFβ was assessed in WT and IFN-β−/− Sham and TBI mice. TBI significantly increased hippocampal mRNA expression of Arg1 (F(1,16) = 11.70, p = 0.0035; F), YM1 (F(1,16) = 6.131, p = 0.0248; G), TGFβ (F(1,16) = 28.69, p < 0.0001; H), and SOCS3 (F(1,16) = 9.001, p = 0.0085; I) in WT and IFN-β−/− mice. There was a genotype effect on YM1 (F(1,16) = 4.737, p = 0.0449) and SOCS3 (F(1,16) = 4.907, p = 0.0416), as well as a significant interaction between TBI and genotype for YM1 (F(1,16) = 4.578, p = 0.0481) and SOCS3 (F(1,16) = 5.153, p = 0.0374). Post hoc analysis demonstrated decreased YM1 and SOCS3 expression in IFN-β−/− TBI mice (YM1: p = 0.0345; SOCS3: p = 0.0273; WT TBI vs IFN-β−/−TBI). Data expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 versus sham (effect of TBI) and +p < 0.05, ++p < 0.01, +++p < 0.001 WT TBI versus IFN-β−/− TBI. Two-way ANOVA (n = 6/group).