Figure 3.

DT and C. diphtheriae cause pyroptosis in a ZAKα and NLRP1-dependent manner but also cause other forms of cell death. (A) Comparison of PI uptake kinetics between control and NLRP1 KO primary keratinocytes in response to purified DT. Error bars represent three biological replicates, with each drug treatment considered as one replicate. Significance values were calculated from Student’s t test at the 7-h time point. **, P ≤ 0.01. (B) Immunoblot of GSDMD, cleaved caspase-3, and IL-1β in WT and NLRP1 KO keratinocyte lysates or media 24 h after the indicated treatment. Immunoblot is representative of three replicate experiments. (C) Comparison of PI uptake kinetics between control and ZAKα KO primary keratinocytes in response to purified DT. Error bars represent three biological replicates, with each drug treatment considered as one replicate. Significance values were calculated from Student’s t test at the 7-h time point. *, P ≤ 0.05. (D) Immunoblot of ZAKα, GSDMD, MCL-1, cleaved caspase-3 and IL-1β in WT and ZAKα KO keratinocyte lysates or media 24 h after the indicated treatment. Salinomycin (10 µM) does not activate the NLRP1 inflammasome and was used as a negative control. Immunoblot is representative of three replicate experiments. Source data are available for this figure: SourceData F3.