As one of the main pathogens of periodontitis, Porphyromonas gingivalis often forms mixed biofilms with other bacteria or fungi under the gingiva, such as Candida albicans. Heme is an important iron source for P. gingivalis and C. albicans that supports their growth in the host. From the perspective of heme competition, this study aims to clarify that the competition for heme enhances the pathogenic potential of P. gingivalis during the interaction between P. gingivalis and C. albicans. Porphyromonas gingivalis single-species biofilm and P. gingivalis-C. albicans dual-species biofilm were established in a low- and high-heme environment. The results showed that the vitality of P. gingivalis was increased in the dual-species biofilm under the condition of low heme, and the same trend was observed under a laser confocal microscope. Furthermore, the morphological changes in P. gingivalis were observed by electron microscope, and the resistance of P. gingivalis in dual-species biofilm was stronger against the killing effect of healthy human serum and antibiotics. The ability of P. gingivalis to agglutinate erythrocyte was also enhanced in dual-species biofilm. These changes disappeared when heme was sufficient, which confirmed that heme competition was the cause of thepathogenicy change in P. gingivalis. Gene level analysis showed that P. gingivalis was in a superior position in the competition relationship by increasing the expression of heme utilization-related genes, such as HmuY, HmuR, HusA, and Tlr. In addition, the expression of genes encoding gingipains (Kgp, RgpA/B) was also significantly increased. They not only participate in the process of utilizing heme, but also are important components of the virulence factors of P. gingivalis. In conclusion, our results indicated that the pathogenic potential of P. gingivalis was enhanced by C. albicans through heme competition, which ultimately promoted the occurrence and development of periodontitis and, therefore, C. albicans subgingival colonization should be considered as a factor in assessing the risk of periodontitis.

作为牙周炎的主要病原体之一， 牙龈卟啉单胞菌 通常与牙龈下的其他细菌或真菌形成混合的生物膜，例如 白色念珠菌。血红素是一种重要的铁来源牙龈卟啉单胞菌 和 白色念珠菌支持他们在主机上的成长。从血红素竞争的角度出发，本研究旨在阐明血红素的竞争增强了血红素的致病潜力。牙龈卟啉单胞菌 在之间的互动 牙龈卟啉单胞菌 和 白色念珠菌。 牙龈卟啉单胞菌 单物种生物膜和 牙龈卟啉单胞菌--白色念珠菌在低血红素和高血红素的环境中建立了双物种生物膜。结果表明，生命力牙龈卟啉单胞菌在低血红素条件下，双物种生物膜中的蛋白含量增加，并且在激光共聚焦显微镜下观察到相同的趋势。此外，在形态上的变化牙龈卟啉单胞菌 用电子显微镜观察， 牙龈卟啉单胞菌在双物种生物膜中，抗健康人血清和抗生素的杀伤作用更强。的能力牙龈卟啉单胞菌双物种生物膜中凝集红细胞的能力也增强了。当血红素足够时，这些变化消失了，这证实了血红素竞争是引起血红蛋白改变的病因。牙龈卟啉单胞菌。基因水平分析表明牙龈卟啉单胞菌通过增加与血红素利用相关的基因（例如HmuY，HmuR，HusA和Tlr）的表达，在竞争关系中处于优势地位。此外，编码姜黄素的基因（Kgp，RgpA / B）的表达也显着增加。它们不仅参与血红素的利用过程，而且还是血红素毒力因子的重要组成部分。牙龈卟啉单胞菌。总之，我们的结果表明，牙龈卟啉单胞菌 被增强 白色念珠菌 通过血红素竞争，最终促进了牙周炎的发生和发展，因此， 白色念珠菌 龈下菌落定植应作为评估牙周炎风险的因素。