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. 2021 Mar 17;12:618577. doi: 10.3389/fimmu.2021.618577

Figure 4.

Figure 4

Protection of neutrophils from rEIII-induced pyroptosis under treatment with Nlrp3 inflammasome inhibitors. Pre-treatments (30 min) with NETosis inhibitor GSK484 (2 nM), Nlrp3 inhibitor OLT1177 (10 μM), and caspase 1 inhibitor Z-WHED-FMK (10 μM) on the rescue of rEIII-induced neutrophil total cell death (A). Pretreatments (30 min) with Nlrp3 inflammasome inhibitors OLT1177, Z-WHED-FMK, and NETosis inhibitor GSK484 rescued rEIII-induced (1 h) neutrophil pyroptosis (B,C), necroptosis (D), autophagy (G) and NETosis (H), but not ferroptosis and apoptosis (E,F). If the respective RCD% was normalized by the population of death cells [(I): dead cell population normalized to 100%], we found that CSB, OLT1177 and Z-WHED-FMK still display rescue effects on pyroptosis (J), necroptosis (K), autophagy (N), and NETosis (O), but not ferroptosis and apoptosis (L,M). Chondroitin sulfate B (CSB, 10 μg/mL), a competitive inhibitor against rEIII binding (33), serving as a positive inhibitor control to inhibit cell death. n = 6, *P < 0.05, **P < 0.01, vs. respective vehicle groups. ND, not detected.