NLRP3炎性小体在感染性疾病中起重要作用，但在弓形虫感染中作用未见报道。我们前期研究发现，弓形虫GRA7蛋白处理人小肠上皮细胞株（FHs 74 Int）后NLRP3蛋白表达明显增多；弓形虫感染可诱导胞内活性氧增加。上述结果提示弓形虫感染或GRA7可能激活NLRP3炎性小体，但激活机制不明。我们推测弓形虫感染可能通过细胞内K+外流、活性氧产生和（或）溶酶体破裂途径激活NLRP3炎性小体，促进IL-18和IL-1β产生。本研究拟用弓形虫直接感染、Transwell侵袭、GRA7蛋白处理FHs 74 Int细胞后，通过基因沉默等方法，在三个层面探讨弓形虫感染所致的细胞内K+外流、线粒体活性氧产生和（或）溶酶体破裂激活NLRP3炎性小体及其交互作用。研究结果将明确NLRP3炎性小体在弓形虫病中作用及其激活机制，深入了解GRA7蛋白的免疫调节作用，为进一步研究肠道寄生虫病的致病机制奠定基础。

NLRP3 inflammasome plays an important role in infectious diseases, but its role in the Toxoplasma gondii infection has not been reported. Our previous study found that after treatment of T. gondii GRA7 protein in a small intestinal epithelial cell (FHs 74 Int)，NLRP3 protein expression was significantly increased; T. gondii infection induced an overexpression of intracellular reactive oxygen species (ROS). These results suggest that T. gondii infection or GRA7 protein might activate NLRP3 inflammasome, but its activation mechanism is unknown. We speculate that T. gondii infection may activate NLRP3 inflammasome via intracellular K+ efflux, mitochondrial ROS generation and/or lysosome rupture, followed by promotion of IL-18 and IL-1β secretion. This project intends to treat FHs 74 Int cell with direct T. gondii infection, Transwell invasion and GRA7 protein, and to determine the role of K+ efflux, mitochondrial ROS production and/or lysosome rupture in NLRP3 inflammasome activation and their interaction using some assays such as gene silencing. Our results will unravel the role and activation mechanism of NLRP3 inflammasome in pathogenesis of toxoplasmosis, understand the immunoregulation of GRA7 protein and lay a foundation for further study of pathogenic mechanism of intestinal parasitosis.