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. Author manuscript; available in PMC: 2017 Jan 2.
Published in final edited form as: Nat Med. 2016 Jul 25;22(9):1002–1012. doi: 10.1038/nm.4153

Figure 1.

Figure 1

Deficiency of NOX4 suppresses NLRP3 inflammasome activation. (a,b) The results of ELISA from LPS-primed WT and Nox4−/− BMDMs for (a) IL-1β, IL-18 and TNF-α after stimulation with nigericin, ATP, silica, MDP or flagellin and (b) for IL-1β after stimulation with poly(dA:dT). (c) Immunoblot analysis for caspase-1 and IL-1β from LPS-primed WT and Nox4−/− BMDMs stimulated with nigericin. (d) Immunoblot analysis for NOX4 in mitochondrial fraction, caspase-1 and IL-1β in cytosolic fraction and (e) ELISA for IL-1β and IL-18 from primary human macrophages transduced with lentivirus expressing two independent NOX4-targeted gRNAs (NOX4 gRNA #1 and NOX4 gRNA #2) and control plasmid (Control), and stimulated with LPS and nigericin or ATP. (f) ELISA for IL-1β, IL-18 and TNF-α and (g) Immunoblot analysis for NOX4 and caspase-1 in lung tissues (100 µg) from WT and Nox4−/− mice after infection of S. pneumoniae or PBS for 24 h (PBS, n = 3 and S. pneumoniae, n = 10). (h) Survival curve of S. pneumoniae infection was determined in WT and Nox4−/− mice (WT, n = 30 and Nox4−/−, n = 30, P = 0.0121 by log-rank test). TOMM20 and β-actin served as the standard. Data are derived from n = 6 (a); n = 3 (b); or n = 6 (c) mice and n = 3 (d) human subjects. All data are mean ± s.d., **P < 0.01 by ANOVA. *P < 0.05 by ANOVA. Data are representative of three independent experiments and each carried out in triplicate.