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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: The FGF/FGFR system in the microglial neuroinflammation with Borrelia burgdorferi: likely intersectionality with other neurological conditions

Fig. 6

Effect of exogenous addition of FGFs on inflammatory mediator output and activation of FGFR1 pathway on primary rhesus microglia. a Various concentrations of recombinant human FGFs were added to enriched primary rhesus microglial (~ 80%) cells for 24 h. PBS/BSA (0.1%) was used as the solvent control. Supernatants were collected and analyzed for IL-6, CXCL8 and CCL2 expression by Multiplex ELISA. Lines within each cytokine/chemokine indicate that they were analyzed separately. 5 ng/ml data is representative of 2 experiments conducted on microglia derived from one frontal cortex tissue, while the higher concentration is representative of 2 experiments conducted on microglia derived from 2 different frontal cortex tissues. Data shown are from experiments that were performed with the same animal tissue. Bar represents standard deviation. Black asterisks represent statistically significant increase over PBS/BSA control. *p < 0.05, **p < 0.01, and ***p < 0.001. b Shows activation of FGFR1 pathway by addition of 5 ng/ml of FGF6 (+ DMSO) to primary rhesus microglial cells. Upregulation of pFGFR1 (green) is seen in cells that also stain for Iba1 (red). Bar represents 50 µm. Panel on the far-right shows the same data at a higher magnification (Bar represents 25 µm). c Shows the effect of PD166866 FGFR1 inhibitor on the inflammatory output in response to exogenous addition of FGF6. A representative experiment is shown of 2–3 experiments carried out on microglia derived from 2 different tissues. Black asterisks represent statistical differences in comparison to FGF6/DMSO control. **p < 0.01

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