Figure 5: TLR2-induces pro-inflammatory processes are inhibited in the presence of glycolytic inhibitor 3PO in vitro.

(a) Representative images displaying RASFC cell invasion (i) (n = 1) and migration (ii) (n = 3) under Pam3CSK4 (1 μg/ml) stimulation (24 hrs) in the presence of absence of 3PO (20 μM) or DMSO vehicle control. (b) Bar graphs demonstrating secretion of IL-6, IL-8, MCP-1, GRO-α and RANTES in RASFC (n = 7) stimulated with Pam3CSK4 (1 μg/ml) for 24 hrs in the presence of absence of 3PO (20 μM) or DMSO vehicle control. (c) Representative cropped western blots demonstrating P-STAT3, Notch-1IC and NFĸBp65 expression in K4IM synoviocytes stimulated with Pam3CSK4 (1 μg/ml) in the presence or absence of 3PO (20 μM) or DMSO vehicle control for 24 hrs (n = 1). T-STAT3 was used as a loading control for P-STAT3 and β-actin was used as a loading control for Notch-1IC and NFĸBp65. Data was analysed by Wilcoxin Signed Rank test and is represented as Mean ± SEM, *p < 0.05, **p < 0.01 significantly different to control.