The rapid formation and activation of the NLRP3 inflammasome is induced by co-stimulation with LPS and nigericin. It requires the LPS-stimulated activation of IKKβ, which exerts its effects independently of de novo gene transcription, protein translation and other protein kinases activated by IKKβ. IKKβ is not required for the nigericin-induced dispersion of the trans-Golgi network (TGN), but to bring NLRP3 in proximity with TGN38. The nigericin-induced dispersion of the Golgi is enhanced by co-stimulation with LPS, and this enhancement is IKKβ-dependent. Prolonged stimulation with LPS to increase the expression of NLRP3, followed by stimulation with nigericin, produced larger TGN38-positive puncta, and the ensuing activation of the NLRP3 inflammasome was also suppressed by IKKβ inhibitors added prior to stimulation with nigericin. IKKβ therefore has a key role in recruiting NLRP3 to the dispersed TGN, leading to the formation and activation of the NLRP3 inflammasome.

中文翻译：

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IKKβ 是 NLRP3 炎性体形成所必需的

NLRP3 炎性体的快速形成和激活是由 LPS 和尼日利亚菌素共同刺激诱导的。它需要 LPS 刺激的 IKKβ 激活，它独立于从头发挥其作用由 IKKβ 激活的基因转录、蛋白质翻译和其他蛋白激酶。尼日利亚菌素诱导的跨高尔基网络 (TGN) 分散不需要 IKKβ，而是使 NLRP3 接近 TGN38。尼日利亚菌素诱导的高尔基体分散通过与 LPS 的共刺激得到增强，这种增强是 IKKβ 依赖性的。用 LPS 延长刺激以增加 NLRP3 的表达，然后用尼日利亚菌素刺激，产生更大的 TGN38 阳性斑点，随后的 NLRP3 炎性体激活也被在用尼日利亚菌素刺激之前添加的 IKKβ 抑制剂抑制。因此，IKKβ 在将 NLRP3 募集到分散的 TGN 中具有关键作用，从而导致 NLRP3 炎性体的形成和激活。