牙龈卟啉单胞菌（Porphyromonas gingivalis, P. gingivalis）为牙周疾病的重要致病菌，感染口腔上皮细胞有其独特的致病机制。前期工作显示，P. gingivalis感染口腔上皮细胞发生细胞周期改变和分化异常，使口腔上皮细胞的防御机能和修复能力发生障碍，其机制主要引起口腔上皮细胞异常增殖和细胞角蛋白表达异常，增强细胞的炎症反应，其中STAT1,3发挥重要的调节作用。本研究拟建立P. gingivalis感染口腔上皮细胞模型，探索STAT1,3/FLI1/KRT途径在调节细胞增殖的过程中，在机体炎症微环境下，启动CSF1/CSF1R和IL6/IL6R，从而增强活化STAT1,3通路，使角蛋白表达发生改变，促进细胞异常增殖和分化，为口腔微生物感染宿主的致病机制研究提供新的视角和分子生物学基础。

Porphyromonas gingivalis, the important pathogenic bacteria in periodontal diseases, could cause infection in oral epithelial cells with the unique pathogenic mechanisms. Preliminary studies showed that inflammatory response caused by P. gingivalis infection resulted in cell cycle disorder and aberrant differentiation, which caused dysfunction in defense and repair ability of oral epithelial cells. STAT1,3 played an important regulatory role. In this study, we aim to establish an oral epithelial cell model infected by P. gingivalis to explore the role of STAT1,3/FLI1/KRT pathway in the regulation of cell proliferation and aberrant differentiation, meanwhile, under the inflammatory microenvironment, CSF1/CSF1R and IL6/IL6R are predicted to be activated to enhance the activation of STAT1,3 in order to regulate the expression of keratins. It would provide a novel perspective and molecular biological evidence for the mechanism of host infection by oral microorganisms.