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. 2016 Jan 22;26(3):367–379. doi: 10.1038/cr.2016.11

Figure 3.

Figure 3

Ablating the expression or kinase activity of PKR suppresses the production of IL-1β and IL-18. (A, B) Production of IL-1β (A) and IL-18 (B) in the culture supernatant of peritoneal macrophages from WT and transgenic mice (eif2ak2−/− and eIF2αk2tm1Lri, n = 3), primed for 4 h with LPS (10 ng/ml) then nigericin (10 μM) for 2 h for IL-1β, or 30 min for IL-18. (C) Assessment of membrane integrity by LDH cytotoxicity assay in the culture supernatant of peritoneal macrophages from WT and transgenic mice (eif2ak2−/− and eIF2αk2tm1Lri, n = 3), primed for 4 h with LPS (10 ng/ml), then nigericin (10 μM) for 30 min. (D) Assessment of TNFα production in the culture supernatant of peritoneal macrophages from WT and transgenic mice (eif2ak2−/− and eIF2αk2tm1Lri, n = 3-4), primed for 4 h with LPS (10 ng/ml), then nigericin (10 μM) for 2 h. (E, F) Production of IL-1β (E) and TNFα (F) in the culture supernatant of peritoneal macrophages from WT mice (n = 3) treated with the PKR inhibitor 2-AP (1 mM) for 1 h before stimulation with LPS (10 ng/ml) for 4 h, then nigericin (10 μM) for 30 min. Cytokine levels are measured by ELISA (*P < 0.05).