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. Author manuscript; available in PMC: 2016 Sep 15.
Published in final edited form as: Immunity. 2015 Sep 1;43(3):451–462. doi: 10.1016/j.immuni.2015.08.008

Figure 3. NLRP3 is required for an ER stress-induced feed-forward loop of mitochondria damage.

Figure 3

≥ Immunoblot of NLRP3 at the mitochondrial fraction of (A) WT and mCAT BMDM and (B) non-targeted (NT) and Txnip-silenced BMDM. (C) Quantitative PCR of mtDNA in cytosolic extracts from RB51-infected WT and Nlrp3−/−, Asc−/−, and z-YVAD-CHO (caspase-1 inhibitor, 2 μM) treated BMDM. (D) IL-1β concentrations in RB51-infected WT and Nlrp3−/−, Asc−/−, and z-YVAD-CHO (caspase-1 inhibitor, 2 μM) inhibited BMDM. Error bars represent mean ± SD of n≥3 independent experiments. *, **, and *** represent p-values of <0.05, <0.001, and <0.0001 respectively. n.s. = not significant. UNT, TM, and LPS+ATP represent untreated, tunicamycin (positive control for ER stress induction, 10 μg/mL), and LPS+ATP (positive control for inflammasome activation, 200 ng/mL and 1mM) respectively. Immunoblots in (A) and (B) are representative of n≥3 independent experiments that were performed and imaged in parallel with identical parameters using a LiCor Odyssey imaging system. See also Supplemental Figure S3.