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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Mucosal Immunol. 2015 Feb 11;8(6):1388–1399. doi: 10.1038/mi.2015.7

Figure 7. ATG16L1-deficient macrophages produce more IL-1β due to increased NLRP3 and caspase-1 activity.

Figure 7

(a) Levels of IL-1β in the supernatants of WT and ATG16L1-deficient macrophages after pretreatment with LPS followed by exposure to Streptolysin O (with 10 mM DTT), Alum, Silica, or ATP. (b) Levels of IL-1β in the supernatants of WT and ATG16L1-deficient macrophages challenged with UTI89 for 24 hours or the NLRP3 activator Alum for 8 hours with or without the Cathepsin B inhibitor CA-074Me. (c) Representative western blot of pro-caspase-1 protein levels normalized to GAPDH values from macrophages at baseline and after 3 hours of UTI89 challenge, quantification (d) displayed normalized to baseline WT levels. A.U., arbitrary units. (e) Level of caspase-1 in the supernatants of macrophages challenged with UTI89 for 24 hours. (f) Level of IL-1β in the supernatants of macrophages challenged with UTI89 for 24 hours with or without a caspase-1 inhibitor during the entire experiment. (g) Level of IL-1β in the supernatants of macrophages challenged with UTI89 for 24 hours with increasing concentrations of glyburide, an NLRP3 inhibitor. *P<0.05, **P<0.01, ***P<0.001. Paired t test (a) or two way ANOVA and bonferroni post test at for each condition (b, d-g). Data are from 3 independent experiments with 3 replicates per experiment (a-b, e-g) or 1 replicate per experiment (d) presented as mean with SEM.