AbM-induced secretion of IL-1β depended upon the NLRP3 inflammasome.

<p>(<b>A</b>) THP-1 cells were stably transfected with shRNAs targeting ASC and NLRP3, and mRNA expression of ASC and NLRP3 was measured by RT-PCR and compared with nontarget control (shCtrl). (<b>B</b>) Knockdown cells were lysed and the protein lysates were subjected to Western blot analysis to confirm decreased protein expression of ASC and NLRP3. β-actin served as the loading control. (<b>C</b>) Knockdown THP-1 cells were treated with AbM at concentrations of 0.1–5% for 24 h, and cell culture supernatants were collected and assayed for IL-1β secretion by ELISA. (<b>D</b>) The cell culture supernatants were analyzed by Western blot analysis using anti-IL-1β antibody. Data are presented as means ± SE of 3 experiments preformed in duplicate. *shCtrl-THP-1 cells versus AbM-untreated shCtrl-THP-1 cells (<i>P</i><0.05). ^#shASC-THP-1 cells versus shCtrl-THP-1 cells (<i>P</i><0.05). ^???shNLRP3-THP-1 cells versus shCtrl-THP-1 cells (<i>P</i><0.05).