Skip to main content
. 2015 May 18;10(5):e0127278. doi: 10.1371/journal.pone.0127278

Fig 2. Francisella priming inflammasome is TLR2 dependent.

Fig 2

Human monocytes were left untreated (NT) or primed for 30 min with TLR2, 4, 5, 6, 9 ligands: Pam3CysSK4 (P3C) (100 ng/ml), Malp2 (M2) (100 ng/ml), PolyI:C (PIC) (10 μg/ml), E. coli endotoxin (LPS) (1 μg/ml), flagellin (Fla) (100 ng/ml) or CpG (10 μg/ml), and then stimulated with ATP (5 mM) for additional 30 min and IL-18 release was measured by ELISA (A). IL-18 release from human monocytes primed for 30 min with 1 μg/ml of LPS from E. coli, F. novicida (Fn) and F. holarctica-LVS (LVS) and stimulated with ATP (5 mM) for 30 min (B). IL-18 release by monocytes, pretreated with TLR2/1 inhibitor CU-CPT (5 and 10 μM) or TLR4 inhibitor RS-LPS (1 μg/ml) for 30 min and then primed with F. novicida (Fn) for 30 min and activated with ATP (5 mM) for 30 min (C). IL-18 release by monocytes preloaded for 30 min with (5 and 10 μM) CU-CPT and incubated with F. novicida (Fn) for 16 h (D). Data represent mean ± SEM, n = 3 independent experiments. * p<0.05. White bars—overnight model, black bars—rapid priming model.