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. Author manuscript; available in PMC: 2017 Feb 25.
Published in final edited form as: Cell. 2016 Feb 25;164(5):896–910. doi: 10.1016/j.cell.2015.12.057

Figure 1. p62, induced on NF-κB activation, suppresses NLRP3-inflammasome dependent IL-1β production.

Figure 1

(A) Immunoblot (IB) analysis of autophagy receptors in wild-type (p62F/F) and p62ΔMye BMDM stimulated with LPS (200 ng/ml). (B) Wild-type BMDM were incubated with or without LPS in the absence or presence of IKKβ inhibitor ML120b and expression of p62, pro-IL-1β, and NLRP3 was IB analyzed. (C) Survival of p62F/F or p62ΔMye mice injected with intraperitoneal (i.p.) LPS (30 mg/kg) without or with anakinra (50 mg/kg), n=11–13. (D, E) 12-weeks old p62F/F or p62ΔMye mice were i.p. injected with LPS and their sera collected 3 hrs later and analyzed by ELISA for TNF (D) and IL-1β (E). (F, H) Release of IL-1β (F) or TNF (H) from LPS-primed p62F/F or p62ΔMye BMDM that were stimulated with the indicated NLRP3 agonists. Data are averages ± s.d. (n=3). (G) IB analysis of caspase-1 and pro-IL-1β processing in LPS-primed WT (W) or p62-deficient (K) iBMDM stimulated as indicated. Data are representative of three independent experiments. *, p<0.05; **, p<0.01; ***, p<0.001.