Figure 1. Aging modulates M1 and M2 MG/MΦ activation genes following TBI.

Quantitative real-time PCR was used to assess the expression levels of classical (M1; A), alternative (M2a; B), acquired deactivation (M2c; C) MG/MΦ activation genes and IL-4 signal transduction pathway (D) genes in cortical tissue from young (3 month old) and aged (24 month old) mice at 24 h post-injury. (A) M1 gene expression levels (IL-1β, TNFα, CD86, iNOS, CCL2 and CCL3) in the aged TBI mice were significantly increased when compared to the young TBI mice (p<0.05 [CCL3], p<0.01 [IL-1β, iNOS, CD86], p<0.001 [TNFα, CCL2]). (B) M2a gene expression levels (Arg-1, Ym1, Mrc) in the aged TBI mice were significantly increased when compared to young TBI mice (p<0.05 [Mrc], p<0.001 [Arg-1, Ym1]). The M2a gene, Fizz-1, was significantly decreased in aged sham mice when compared to young sham mice (p<0.001), and TBI resulted in significantly reduced Fizz-1 expression in young mice (p<0.01). (C) M2c gene expression levels (IL-4Rα, SOCS3, TGFβ) were significantly increased in young TBI mice when compared to young sham mice (p<0.001), and expression levels were significantly lower in aged TBI mice when compared with young TBI mice (p<0.01 [IL-4Rα], p<0.001 [SOCS3, TGFβ]). (D) STAT 6 expression was significantly increased in the young TBI mice when compared to young sham mice (p<0.01), and STAT6 expression was significantly lower in aged TBI mice when compared to young TBI mice (p<0.05). Statistical analysis was by two-way ANOVA (injury x aging), followed by post-hoc adjustments using Student-Newman-Keuls Multiple Comparison test; *p<0.05, +p<0.05, ##p<0.01, ++p<0.01, ^^p<0.01, +++p<0.001, ###p<0.001 and ***p<0.001, where + = TBI 3 month vs. sham 3 month, * = TBI 24 month vs. sham 24 month, # = TBI 3 month vs. TBI 24 month, ^ = sham 3 month vs. sham 24 month. Bars represent mean ± s.e.m.