Inflammasomes are cytosolic innate immune complexes, which assemble in mammalian cells in response to microbial components and endogenous danger signals. A major family of inflammasome activators is bacterial toxins. Inflammasome sensor proteins, such as the nucleotide‐binding oligomerisation domain‐like receptor (NLR) family members NLRP1b and NLRP3, and the tripartite motif family member Pyrin⁺ efflux triggered by pore‐forming toxins or by other toxin‐induced homeostasis‐altering events such as lysosomal rupture. Pyrin senses perturbation of host cell functions induced by certain enzymatic toxins resulting in impairment of RhoA GTPase activity. Assembly of the inflammasome complex activates the cysteine protease caspase‐1, leading to the proteolytic cleavage of the proinflammatory cytokines IL‐1β and IL‐18, and the pore‐forming protein gasdermin D causing pyroptosis. In this review, we discuss the latest progress in our understanding on the activation mechanisms of inflammasome complexes by bacterial toxins and effector proteins and explore avenues for future research into the relationships between inflammasomes and bacterial toxins.

中文翻译：

---

细菌毒素激活炎症小体的机制

炎性体是细胞溶质的先天免疫复合物，它们在哺乳动物细胞中组装以响应微生物成分和内源性危险信号。炎症小体激活剂的一个主要家族是细菌毒素。炎性体传感器蛋白，例如核苷酸结合寡聚化结构域样受体 (NLR) 家族成员 NLRP1b 和 NLRP3，以及三联基序家族成员 Pyrin ⁺由成孔毒素或其他毒素诱导的体内平衡改变事件（如溶酶体破裂）触发的流出。Pyrin 感知由某些酶毒素诱导的宿主细胞功能扰动，从而导致 RhoA GTPase 活性受损。炎性体复合物的组装激活半胱氨酸蛋白酶 caspase-1，导致促炎细胞因子 IL-1β 和 IL-18 的蛋白水解裂解，以及导致细胞焦亡的成孔蛋白 gasdermin D。在这篇综述中，我们讨论了我们对细菌毒素和效应蛋白激活炎症小体复合物的理解的最新进展，并探索了未来研究炎症小体和细菌毒素之间关系的途径。