NOX4-dependent fatty acid oxidation promotes NLRP3 inflammasome activation in macrophages

ctss − / − macrophages, caspase inhibition still reduced IL-1β levels in both peritoneal macrophages and BMDMs (Fig. Next we compared intracellular caspase 1 activity in

Similar to transduction with Fasn shRNA, knockdown of FASN by Fasn-specific siRNA markedly reduced Nlrp3, Il1b, and Il18 gene expression in response to LPS compared with con-

Similar to transduction with Fasn shRNA, knockdown of FASN by Fasn-specific siRNA markedly reduced Nlrp3, Il1b, and Il18 gene expression in response to LPS compared with con-

Administration of AC-YVAD-CMK, a caspase-1 inhibitor, reduced the expression of IL-1 β and IL-18 and the number of PI-positive cells, attenuated brain edema, and improved

However, targeting MARK4/NLRP3 interaction or loss of MARK4 significantly affects NLRP3 inflammasome transport, positioning on MTOC, ASC oligomerization, and levels of caspase-1 and

ness of A498 cells was significantly decreased following UA treatment (P<0.05), while expression levels of NLRP3, cleaved caspase‑1 and IL‑1 β were significantly increased, and

Importantly, DHA administration or Nlrp3 deficiency blocked HFD-induced IL-1b or IL-18 production and caspase-1 activation in these tissues ( Figures 7 A–7D, 7I), indicating that

Additional MAVS deletion in Stat1 -/- macro- phages did not alter inflammasome responses in terms of caspase-1 cleavage ( Fig 4E ), consis- tent with its dispensable role in