Fig. 3

TgM83^+/− mice display early and late inflammatory responses in the brain after MCAO. Microglia and astrocytes in coronal brain tissue sections of MCAO- and sham-treated TgM83^+/− mice were stained with antibodies to Iba1 or to GFAP, respectively (a). Quantification of the stainings revealed that microgliosis (b) and astrogliosis (c) were significantly induced at 14 days post surgery within the stroke lesion area of mice subjected to MCAO (dark red) when compared to the contralateral hemisphere (light red), or the ipsi- (dark blue) and contralateral (light blue) brain hemispheres of sham-treated animals. Beginning at 30 days post surgery we measured a continuous decline in the level of inflammation, which was reduced to levels observed in sham-treated animals at 90 days post surgery for astrogliosis and later at 180 days post surgery for microgliosis. Following its initial clearance, the inflammatory reaction, surprisingly, began to resurface again in the brains of MCAO-treated animals. We measured a continuous rise of astrogliosis from 90 to 360 days post surgery in the ipsilateral brain hemisphere of MCAO-treated animals. At 360 days post surgery also microgliosis was significantly induced again in the ipsilateral and, importantly, also in the contralateral brain hemisphere of MCAO-treated animals. A continuous increase of astrogliosis was also measured in the contralateral brain hemisphere of MCAO-treated animals at 180 and 360 days post surgery but did not reach significance. The data represent the mean area fraction in percent ± standard deviation. Six to twelve coronal brain sections of three to five animals were analyzed per group at 14, 30, 180, and 360 days post surgery. P values were computed using two-way ANOVA followed by Tukey’s post-hoc test (P: * < 0.05, **** < 0.0001). Scale bars represent 1.0 mm