Cholestasis is a common complication of sepsis, and the increased plasma levels of bile acids are predictive of sepsis-associated mortality. 胆汁淤积是脓毒症的常见并发症，血浆中胆汁酸水平的升高是预测脓毒症相关死亡的指标。 However, the exact mechanism by which cholestasis aggravates sepsis development remains elusive. 然而，胆汁淤积如何加剧脓毒症发展的确切机制尚不明确。 Here, we show that bile acids are danger-associated molecular patterns (DAMPs) that can activate both signal 1 and 2 of the NLRP3 inflammasome in inflammatory macrophages. 在这里，我们展示了胆汁酸是危险相关分子模式（DAMPs），能够在炎症性巨噬细胞中激活NLRP3炎症体的信号1和2。 Mechanistically, bile acids induce a prolonged calcium influx and activate the NLRP3 inflammasome synergistically with ATP. 在机制上，胆汁酸引起持续的钙离子内流，并与ATP协同激活NLRP3炎症体。 Experimental cholestasis sensitizes, while cholestyramine, a bile acid sequestrant, protects mice from LPS-induced sepsis. 实验性胆汁淤积使小鼠对脂多糖（LPS）诱导的脓毒症更为敏感，而胆酸结合剂胆砂胶则能保护小鼠免受LPS诱导的脓毒症。 FXR negatively regulates the NLRP3 inflammasome via physical interaction with NLRP3 and caspase 1. Fxr-null mice are more sensitive, while FXR-overexpressing mice are more resistant, to endoxemia shock. 法尼酯体X受体（FXR）通过与NLRP3和caspase 1的物理相互作用负向调节NLRP3炎症体。缺乏FXR的小鼠对内毒素性休克更为敏感，而过表达FXR的小鼠则更为抵抗。 These findings suggest that bile acids and FXR play pivotal roles in sepsis via controlling the NLRP3 inflammasome, and that targeting FXR may represent a therapeutic strategy for cholestasis-associated sepsis. 这些发现表明，胆汁酸和FXR通过控制NLRP3炎症体在脓毒症中发挥关键作用，并且以FXR为目标可能代表胆汁淤积相关脓毒症的治疗策略。