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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Microglia as target for anti-inflammatory approaches to prevent secondary brain injury after subarachnoid hemorrhage (SAH)

Fig. 5

Receptor surface expression of TLR4 and CD115. One known mechanism of inflammation is the TLR4 pathway. a TLR4 gene expression in isolated microglia was evaluated using qPCR. No significant changes of gene expression levels were seen at days 4 and 14 after the bleeding (n.s.). b As internalization of TLR4 is a potential mechanism of LPS preconditioning, the relative amount of TLR4 on the surface of microglia was determined using FACS-staining (d4). While TLR4-levels on microglia of Sham and SAH-animals were comparable (n.s.), in LPS-preconditioned animals significantly lower numbers of microglia presenting TLR4 on their surface were found, supporting the proposed mechanism of TLR4 internalization upon the inflammatory stimulus. (Proportion of microglia presenting TLR4 on their surface: Sham 11.5%, SAH 11.3%, LPS preconditioning 5.7%, p < 0.01 vs. both other groups). c As a proof of concept for pharmacological microglia deactivation by PLX3397, FACS-staining was performed for microglia positive for CSF1R (CD115). A significant decrease of CD115+ microglia was detected after PLX3397 treatment, when compared to both other groups (Proportion of microglia presenting CSF1R on their surface: Sham 16.9%, SAH 17.3%, PLX3397 treatment 8.8%, p < 0.01 vs. both other groups). n = 6 per group, ANOVA: **p < 0.01

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