目的:探讨NOD样受体蛋白3(NOD-like receptor protein 3，NLRP3)对巨噬细胞吞噬创伤弧菌能力的影响和调控机制。方法:转录组测序分析创伤弧菌感染J774A.1细胞吞噬相关基因的表达谱；CRISPR-Cas9基因编辑技术构建NLRP3敲除(NLRP3 KO)的J774A.1细胞；流式细胞术分析未敲除J774A.1和NLRP3 KO J774A.1细胞对创伤弧菌和pHrodo RED标记的大肠埃希菌(n Escherichia coli，n E.n coli)修饰微球的吞噬能力；荧光定量PCR检测吞噬相关基因n Fgr2n b的表达情况。n 结果:J774A.1细胞感染创伤弧菌后，吞噬功能相关基因表达谱中约有18个基因表达上调(n P<0.05)；NLRP3 KO J774A.1细胞在NLRP3的第2个外显子中有5个碱基的缺失，发生移码突变，导致NLRP3表达缺陷；创伤弧菌或n E.n coli修饰微球体外作用后，NLRP3 KO J774A.1细胞较未敲除组吞噬能力均显著增强，差异有统计学意义；与未敲除组比较，创伤弧菌感染的NLRP3 KO J774A.1细胞中n Fgr2n b基因的表达显著升高，差异有统计学意义。n 结论:NLRP3能负调控巨噬细胞对创伤弧菌的吞噬功能，其作用机制可能与调控吞噬相关基因n Fgr2n b的表达有关。n “,”Objective:To investigate the role of NOD-like receptor protein 3 (NLRP3) in the regulation of phagocytosis in n Vibrio vulnificus (n V.n vulnificus)-infected macrophages.n Methods:Expression profiles of phagocytosis-related genes in PBS- and n V. n vulnificus-infected J774A.1 cells were analyzed by RNA-Seq. NLRP3-knockout (NLRP3 KO) J774A.1 cells were constructed using CRISPR-Cas9 gene-editing system. The phagocytosis of n V. n vulnificus and pHrodo RED-labelled n Escherichia coli (n E.n coli) bioparticles in parental and NLRP3 KO J774A.1 cells was detected by flow cytometry. Real-time PCR was performed to measure the expression of n Fgr2n b gene at mRNA level in PBS- and n V. n vulnificus-treated parental and NLRP3 KO J774A.1 cells.n Results:The expression of 18 phagocytosis-related genes was upregulated in n V. n vulnificus-infected J774A.1 cells than in PBS-treated J774A.1 cells (n P<0.05). There was a 5 bp deletion in the exon 2 of NLRP3 gene in NLRP3 KO J774A.1 cells, resulting in frameshift mutation and complete loss of NLRP3 expression. NLRP3 KO J774A.1 cells exhibited enhanced phagocytosis ofn V. n vulnificus and pHrodo RED-labelled n E. n coli bioparticles than parental J774A.1 cells (n P<0.05). Besides, the expression ofn Fgr2n b gene at mRNA level was significantly increased in n V. n vulnificus-infected NLRP3 KO J774A.1 cells than in parental J774A.1 cells (n P<0.05).n Conclusions:The phagocytosis of n V. n vulnificus in macrophages could be negatively regulated by NLRP3, which was possibly mediated through the regulation of n Fgr2n b gene expression.n