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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Deletion of p38α MAPK in microglia blunts trauma-induced inflammatory responses in mice

Fig. 5

TBI-induced persistent alterations in microglial morphology are mitigated by knockout of p38α in microglia. Tissue sections spanning the ipsilateral peri-contusion cortex and dorsal hippocampal formation were quantified for the positive staining area of Iba1 at the 7 days post-injury interval. Using a pixel-positive algorithm, we observed a lessened reactivity with Iba1+ area in both the peri-contusion (a) and dorsal hippocampus CA1 molecular layer (b) for injured KO mice, relative to injured WT. Morphologically, Iba1 staining appeared to have increased amoeboid phenotype in the injured cortex of WT mice, relative to injured KO. Similarly, there was a visual trend for hippocampal microglia to have larger soma in injured WT mice, compared to KO. In both the cortex (a) and hippocampus (b), p38α KO mice subjected to TBI had a significantly reduced Iba1+ area fraction compared to their WT controls. Data were analyzed using two-way ANOVA with Sidak’s multiple comparison corrections on the pre-planned contrasts examining the effect of TBI in the WT versus KO conditions. **p < 0.01, comparing KO (blue bars) to WT (orange bars)

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