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Fig. 1 | Fluids and Barriers of the CNS

Fig. 1

From: Streptococcus agalactiae disrupts P-glycoprotein function in brain endothelial cells

Fig. 1

GBS effects on iPSC-derived BEC P-gp function. a BECs were either uninfected (control) or infected with GBS (MOI = 10) for 5 h. After infection, P-gp activity was measured by observing R123 accumulation with or without CsA inhibition. b P-gp activity measured using FLUO-3-AM as a P-gp substrate. Experimental groups and infection times are as described in (a). c Just as in (a), BECs were either left uninfected (control) or infected with GBS (MOI = 10) for 5 h. P-gp activity was measured by observing R123 accumulation with or without PSC-833 (PSC) as the inhibitor d. P-gp activity assay monitoring R123 accumulation as in (a) for BECs incubated with non-pathogenic L. lactis (MOI = 10) for 5 h. e BECs tested for R123 accumulation after treatment with the P-gp inhibitor CsA, BCRP inhibitor Ko143, and MRP family inhibitor MK571. Experiments were performed at least in triplicate on three independent differentiations (ac, e, n = 9), or in triplicate on two independent differentiations (d, n = 6). All data are presented, and expressed as % of uninfected control BEC accumulation for all experiments, and bars represent mean ± SD. **p < 0.01, ***p < 0.001, NS p > 0.05, versus uninfected control; ANOVA followed by Dunnett’s multiple comparisons test

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