FIGURE 3.

Lipotoxic inflammasome activation requires saturated fatty acids independently of high glucose or ATP. A–C, IL-1β concentration in the media was determined 20 h after stimulation of pMACs with the indicated FFA (stearate (stear) or oleate (ole) (A)), in the presence or absence of 1 μm triascin C (TC (B)), or in high (4.5 g/liter) or low (1g/liter) glucose medium (C). D, macrophages were treated with palmitate (palm)-LPS for 20 h ± apyrase or primed with LPS for 2 h followed by 5 mm ATP ± apyrase for 60 min, and IL-1β release was quantified by ELISA. E, pMACs were treated with palmitate-LPS simultaneously (S) or pretreated with LPS for the indicated times followed by palmitate incubation for 20 h. As a control, the cells were also treated with LPS for 2 h followed by silica (200 μg/ml) for 6 h. IL-1β concentration in the supernatant was determined by ELISA. Bar graphs indicate the means ± S.E. for a minimum of three experiments, each performed in triplicate. *, p < 0.05 for BSA-PBS versus FFA-LPS, or vehicle (veh) versus inhibitor. ns, not significant.