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. 2014 Oct 6;289(47):32926–32936. doi: 10.1074/jbc.M114.579961

FIGURE 3.

FIGURE 3.

The TAK1-JNK pathway regulates NLRP3 inflammasome activation. A and B, lysates from THP-1 macrophages stimulated with LLME for the indicated times in the absence (A) or presence of calyculin A (B) were immunoblotted with antibodies against p-TAK1 and TAK1. C, lysates from THP-1 macrophages stimulated with LLME for the indicated times in the absence or presence of Oxozeaenol were immunoblotted with antibodies against p-MAPKs, MAPKs, and IκBα. DMSO, dimethyl sulfoxide. D and E, LPS-primed THP-1 macrophages were subjected to LLME stimulation for 3 h with the indicated inhibitors, such as Oxozeaenol (0.5 μm, Oxo), SP600125 (10 μm, SP), SB202190 (10 μm, SB), and Bay11-7082 (10 μm, Bay). The culture supernatants were collected and immunoblotted with antibodies against caspase 1 p10 and cleaved IL-1β. F, mice were challenged intraperitoneally with 3 mg of MSU crystals at 1 h after TAK1 inhibitor administration. The number of neutrophils in the peritoneal cavities at 6 h after injection of the MSU crystals was plotted. *, p < 0.05. The results are representative of at least three (A, C, D, and F) and two (B and E) independent experiments.