Fig. 5

Lipopolysaccharide-stimulated MP activate BV2 microglia. a Enriched MP were isolated from control and LPS-stimulated BV2 microglia and were co-cultured with naïve BV2 microglia for 24 h. Pro-inflammatory mediators (IL-1β, TNF-α, miR-155, IL-6, CCL2, and NOS2) were significantly increased in BV2 microglia treated with LPS MP (*p < 0.05 and ***p < 0.001 vs naïve; ^^p < 0.01 and ^^^p < 0.001 vs control MP; one-way ANOVA with Student-Newman-Keuls correction for multiple comparisons; n = 4/group). Data represent results of three independent experiments. b MP neutralization using PEG-TB. Enriched MP from control and LPS-stimulated BV2 microglia were incubated with increasing concentrations of PEG-TB for 1 h, and number of MP were quantified by flow cytometry. 6 μl PEG-TB/100 μl resulted in significant depletion of MP under both conditions. c Naïve BV2 microglia were co-cultured with control or LPS-stimulated MP ± PEG-TB (6 μl/100 μl) for 24 h. LPS MP treatment increased IL-1β and TNF-α in BV2 microglia (**p < 0.01 and ***p < 0.001 vs control MP), whereas co-treatment with PEG-TBI resulted in a significant decrease in IL-1β and TNF-α expression (^^^p < 0.001 vs LPS MP; one-way ANOVA with Student-Newman-Keuls correction for multiple comparisons; n = 6/group). Bars represent mean ± S.E.M.