NLRP3 (NOD-, LRR- and pyrin domain- containing protein 3) inflammasome is involved in diverse inflammatory diseases, so the activation of NLRP3 inflammasome needs to be tightly regulated to prevent excessive inflammation. However, the endogenous regulatory mechanisms of NLRP3 inflammasome are still less defined. Here, we report that β-catenin, which is the central mediator of the canonical Wnt/β-catenin signaling, promotes NLRP3 inflammasome activation. When we suppressed the expression of β-catenin by siRNA or pharmacological inhibitor, the NLRP3 inflammasome activation was impaired. Accordingly, β-catenin inhibitor attenuated LPS-induced systemic inflammation in vivo. Mechanistically, we found β-catenin interacted with NLRP3 and promoted the association between NLRP3 and ASC. Thus, our study revealed a novel role of β-catenin in NLRP3 inflammasome activation and suggest an endogenous crosstalk between Wnt/β-catenin signal and NLRP3 inflammasome.

中文翻译：

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β-catenin通过增加NLRP3与ASC之间的结合来促进NLRP3炎性体活化。

NLRP3（含NOD，LRR和吡喃结构域的蛋白质3）炎性小体与多种炎性疾病有关，因此需要严格调节NLRP3炎性小体的激活，以防止过度炎症。但是，NLRP3炎性小体的内源性调节机制仍不清楚。在这里，我们报道β-catenin，这是经典的Wnt /β-catenin信号传导的中心介质，可促进NLRP3炎性体激活。当我们通过siRNA或药理抑制剂抑制β-catenin的表达时，NLRP3炎性体的激活受到损害。因此，β-连环蛋白抑制剂在体内减轻了LPS诱导的全身炎症。从机理上讲，我们发现β-catenin与NLRP3相互作用并促进了NLRP3与ASC之间的结合。从而，