Fig. 6

P2X7 receptor stimulation impairs the NLRP3 inflammasome in monocytes. a, b Percentage of monocytes with ASC-specks (a) and release of IL-1β from PBMCs (b) isolated from healthy donor blood samples treated with ATP (3 mM, 30 min; ATP-pre), then washed and primed with or without LPS (1 μg/ml, 2 h) and then treated for 20 min with ATP (3 mM; ATP-post) or nigericin (10 μM) as indicated. c IL-1β release from wild type or P2rx7^−/− BMDMs treated as in a, but with 4 h LPS priming and 30 min of ATP or nigericin. d IL-1β release from wild type or P2rx7^−/− BMDMs treated for 30 min with antimycin A (5 μM) or FCCP (1 μM), and then washed and primed with LPS (1 μg/ml, 4 h) and then stimulated with nigericin (10 μM, 30 min) as indicated. e Expression of Nrlp3 and Il1b genes analyzed by quantitative PCR from wild type or P2rx7^−/− BMDMs treated with ATP (3 mM, 30 min; ATP-pre), then washed and primed with or without LPS (100 ng/ml, 4 h). f Kaplan–Meier representation of wild type (top) or P2rx7^−/− (bottom) mice survival after sham operation (dotted line), or CLP operation (continuous line); some mice groups were i.p. injected with ATP (0.5 mg/g) 30 min before operation (dashed lines). Wild type CLP n = 10, CLP + ATP n = 8, sham n = 4, sham + ATP n = 4; P2rx7^−/− CLP n = 4, CLP + ATP n = 6, sham n = 3. g IL-1β from peritoneal lavage (left) or bacterial load in blood (right) from wild type sham, CLP or CLP+ATP mice after 24 h. Each dot represents a single independent experiment (c, d), a sample from an individual healthy donor (a, b, e) or a single mouse (g); average ± standard error is represented in panels a–e, g; exact n number for each panel is presented in Source Data file; *p < 0.05; **p < 0.01; ns, no significant difference (p > 0.05); Mann–Whitney test was used for a, b, d, e; Kruskal–Wallis test was used for c; Log-rank test for f