The inflammatory response is a complex regulated effector mechanism of the innate immune system that is initiated after tissue injury or infection. The NLRP3 inflammasome is an important initiator of inflammation by regulating the activation of caspase-1, the maturation of pro-inflammatory cytokines and the induction of pyroptotic cell death. Numerous studies demonstrate that the NLRP3 inflammasome could be modulated by lipids, existing a relation between lipids and the activation of different inflammatory processes. In this review we will summarize how the mechanism of NLRP3 inflammasome activation is regulated by different lipids and how these lipids control specific cellular localization of NLRP3 during activation. Although being a cytosolic protein, NLRP3 interacts with lipids accessible in neighbor membranes. Also, the modulation of NLRP3 by endogenous lipids has been found causative of different metabolic diseases and bacterial-pathogenic lipids lead to NLRP3 activation during infection. The understanding of the modulation of the NLRP3 inflammasome by lipids has resulted not only in a better knowledge about the mechanism of NLRP3 activation and its implication in disease, but also opens a new avenue for the development of novel therapeutics and vaccines, as NLRP3 could be modulated by synthetic lipids used as adjuvants.

炎症反应是先天免疫系统的复杂调节效应机制，在组织损伤或感染后启动。NLRP3 炎症小体是炎症的重要引发剂，通过调节 caspase-1 的激活、促炎细胞因子的成熟和诱导焦亡细胞死亡。大量研究表明NLRP3炎症小体可以通过脂质调节，脂质与不同炎症过程的激活之间存在关联。在这篇综述中，我们将总结不同脂质如何调节NLRP3炎症小体激活的机制，以及这些脂质如何在激活过程中控制NLRP3的特定细胞定位。尽管 NLRP3 是一种胞质蛋白，但它与邻近细胞膜中的脂质相互作用。还，已发现内源性脂质对 NLRP3 的调节会导致不同的代谢疾病，并且细菌致病性脂质会在感染期间导致 NLRP3 激活。对脂质对 NLRP3 炎性体的调节的了解不仅使人们更好地了解 NLRP3 激活机制及其在疾病中的意义，而且还为开发新型疗法和疫苗开辟了新途径，因为 NLRP3 可以由用作佐剂的合成脂质调节。