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

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Copyright © 2021 Lien, Sun, Hung, Wu and Chang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Nlrp3 and caspase 1 deficiencies protest rEIII-induced neutrophil ROS production and NETosis. Treatments (1 h) of rEIII (0.6 μM)-induced elevations of neutrophil cellular reactive oxygen species (ROS) (A) hydrogen peroxide (B), superoxide (C) in vitro. Treatments (1 d) of rEIII (2 mg/kg)-induced elevations of circulating CitH3 (D) levels in wild type mice. By contrast, such rEIII (0.6 μM in vitro, 2 mg/kg in mice)-induced stimulations are markedly reduced in Nlrp3^−/− and Casp1^−/− gene knockout mice in both in vitro and in vivo experiments (A–D). n = 6, ^#P < 0.05, ^##P < 0.01, vs. respective wild type (WT) groups; *P < 0.05, **P < 0.01, vs. respective vehicle groups.