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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Microglia amplify inflammatory activation of astrocytes in manganese neurotoxicity

Fig. 7

Glial crosstalk in Mn toxicity relies on NF-κB signaling in microglia. Prior to use in MCM experiments, microglia or BV2 microglia cells were pretreated with the NF-κB inhibitor Bay11 or DMSO. a Suppression of NF-κB-driven expression of Nos2 was assessed in BV2 microglial cells treated with lipopolysaccharide (1 μg/mL) for 24 h. Suppression of NF-κB-regulated inflammatory genes in microglia was measured via qPCR for Nos2 (b), Tnf (c), and caspase 1 (d). Representative image (e) from the Quansys mouse 14-plex array indicating location of noted chemokines and cytokines. (f) Representative heat maps of Quansys multi-plex ELISA results of media from 0 or 100 μM MnCl2-treated microglia in combination with DMSO or Bay11 with dot locations correlating to e. Intensity is represented by no expression (blue) to increasing expression (yellow). Levels of TNF (g), IL-6 (h), CCL2 (i), and CCL5 (j) were calculated based on standard curves generated during experiments. Levels of inflammatory gene expression in astrocytes treated with MCM versus MCM of microglia treated with DMSO or Bay11 were determined via qPCR for Tnf (K), Il-1β (l), Il-6 (m), Ccl2 (n), and Ccl5 (o). Expression data is represented by mRNA fold change ± SEM while ELISA data is represented by mean concentration (pg/mL) ± SEM (one-way ANOVA; asterisks above bars indicate significance from control; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001)

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