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. 2022 Sep 14;8(37):eabo5400. doi: 10.1126/sciadv.abo5400

Fig. 2. NIC inhibits multiple inflammasomes.

Fig. 2.

BMDMs were primed with LPS (500 ng/ml) for 3 hours; treated with vehicle (V) or NIC at 10 μM for 1 hour; and then left nontreated (NT) or stimulated with nigericin (20 μM) or poly(dA:dT) (5 ng/ml) or left noninfected (NI) or infected with WT L.p. (MOI of 10) or flaA− L.p. (MOI of 10). Western blot analysis showing caspase-1 p20 and IL-1β cleavage p17 in cell-free SNs and caspase-1 p45, IL-1β p31, and β-actin p43 in the cellular extract (CE) after stimulus with (A) nigericin (20 μM) or transfected with (B) poly(dA:dT) (5 ng/ml) or infected with (C) WT L.p. (MOI of 10) or (D) flaA− L.p. (MOI of 10). LPS-primed BMDMs were treated with 1, 3, or 10 μM NIC for 1 hour and then left NT or stimulated with nigericin (20 μM) or poly(dA:dT) (5 ng/ml) or left NI or infected with WT L.p. (MOI of 10) or flaA− L.p. (MOI of 10). SNs were assayed for (E) an IL-1β release or (F) a caspase-1 activity using the Caspase-1 Glo kit assay. The percentage of cell containing (G) NLRP3 puncta after nigericin treatment, (H) ASC puncta after WT L.p., or (I) ASC puncta after flaA− L.p. infection was estimated in cells. *P < 0.05, compared to vehicle; n.s., nonsignificant as determined by Student’s t test. Data are presented from one representative experiment of three experiments performed with similar results.