Fig. 4

C3 inhibits NLRP3 inflammasome activation independently of GPCRs and HDAC inhibitor, while C4 is dependent on the GPR109A receptor. BMDMs (LPS-primed) treated with propionate (C3, 3 mmol/L), butyrate (C4, 0.5 mmol/L), TSA (50 nmol/L), Panobinostat (25 nmol/L), AR42062 (25 μmol/L), 4-CMTB (100 μmol/L), niacin (1 mmol/L) and then stimulated with CoCrMo alloy particles. Supernatants were analysed by immunoblotting for caspase-1, IL-1β activation (a), and assayed for IL-1β secretion (b). BMDMs (LPS-primed) from wild type (WT) and GPR109A^−/− mice treated with C3 or C4 and then stimulated with CoCrMo alloy particles. Supernatants were analysed by immunoblotting for caspase-1, IL-1β activation (c), and assayed for IL-1β secretion (d). Results are mean ± SEM, ^**P < 0.01,^***P < 0.001, ns non-significant. C3 propionate, C4 butyrate, IL-1β interleukin 1 beta, LPS lipopolysaccharide, TSA trichostatin A