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. 2016 Dec 2;12(12):e1006035. doi: 10.1371/journal.ppat.1006035

Fig 1. The Y. pestis effector YopM suppresses a different IL-1β-producing pathway than the one triggered by the needle/translocon through NLRP3 and NLRC4.

Fig 1

IL-1β in supernatants from A) WT LPS-primed BMDMs infected with Y. pestis Yop mutant strains, B) BMDMs of indicated genotypes infected with ΔT3SSe, or C) LPS-primed BMDMs infected with KIM5 and ΔYopM were measured by ELISA 6 hrs p.i. (MOI 10). D) Cell death was assayed by LDH release in LPS-primed BMDMs infected with indicated strains at 6 hrs p.i. (MOI 10). Figures are representative of three or more experiments. E) Total protein from LPS-primed BMDMs infected with indicated strains (combined cell lysate and supernatant) was separated by SDS-PAGE and analyzed by Western Blot for IL-1β and caspase-1. F) Mice of indicated genotypes were injected s.c. with 160 CFU of KIM1001ΔM/J and monitored for survival past 21 days. P value for survival comparisons reflect differences between WT (n = 11) or NLRP3 KO (n = 11) and IL-18 (n = 6), Asc KO (n = 14). Shown is mean plus s.d. for triplicate wells. ND: not detected. A-E are representative of three experiments or more, F representative of two experiments performed. * p<0.05, **p<0.01, ***p<0.001.