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. Author manuscript; available in PMC: 2012 Jul 15.
Published in final edited form as: J Immunol. 2011 Jun 15;187(2):613–617. doi: 10.4049/jimmunol.1100613

Figure 2. Inhibitors of the ROS system block NLRP3-mediated caspase-1 activation byinhibiting cell priming.

Figure 2

A, wild type macrophages were pretreated for 1 h with DPI (20 μM), NAC (20 mM), Cytochalasin D (5 μM) or Bafilomycin (250 nM), thenstimulated as indicatedand subsequently assessed for cleavage ofcaspase-1. B, wild type macrophages were pretreated for 1 h with 0, 10 or 20 μM DPI, then stimulated as indicated and subsequently IL-18 release was measured by ELISA. C, wild type macrophages were treated with ascending doses of DPI, subsequently primed with LPS and then assessed for NLRP3 mRNA expression. D and E, wild type macrophages were treated with DPI (1h) and then primed with LPS (3h) or alternatively, macrophages were primed with LPS (3h), then treated with DPI (1h) and subsequently stimulated as indicated. 6 h following stimulation IL-1β and IL-18 release were assessed in the supernatant. F, Cleaved caspase-1 of wild type and NLRP3-deficient macrophages reconstituted with NLRP3 is depicted. Data from one representative experiment of two (A, B, D and E) or three (C and F) are presented.