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Lipopolysaccharide from Escherichia coli but not from Porphyromonas gingivalis induce pro-inflammatory cytokines and alkaline phosphatase in dental follicle cells

机译:来自大肠杆菌的脂多糖而不是来自牙龈卟啉单胞菌的脂多糖诱导牙囊细胞中促炎性细胞因子和碱性磷酸酶

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Objectives: Dental follicle cells (DFCs) as periodontal precursor cells are the natural source for cellular therapies of periodontitis. Periodontitis is initiated after the infection of the periodontium with oral pathogens such as the Gram-negative bacteria Porphyromonas gingivalis. Lipopolysaccharide (LPS) is the major component of the outer membrane of gram-negative bacteria. Previous studies have shown that especially P. gingivalis LPS induces the expression of pro-inflammatory cytokines in PDL cells and disturbs the differentiation of dental stem cells. Our study investigated the administration of LPS to DFCs for the first time. Materials and methods: We evaluated cell proliferation (WST1 assay), expression of cytokines IL1β, IL8 and IL6 (real-time RT-PCR) and the osteogenic differentiation of DFCs (ALP-activity and Alizarin red staining) in the presence of P. gingivalis LPS and Escherichia coli LPS. Results: All tested pro-inflammatory cytokines were highly increased after E. coli LPS treatment. P. gingivalis LPS induces only the expression of IL8, but this expression was significantly lower than that after E. coli LPS administration. The ALP activity was significantly higher in DFCs after the administration of E. coli LPS than after administration of P. gingivalis LPS or under normal cell differentiation conditions. However, the mineralization was inhibited with LPS from both bacterial species. Conclusion: LPS disturbs osteogenic differentiation in DFCs. Moreover, the failure of pro-inflammatory cytokines induction in DFCs after the administration of P. gingivalis LPS differs greatly from that of PDL fibroblasts. These immunological properties of DFCs have to be considered for cellular therapies of periodontitis with DFCs.
机译:目的:牙周细胞的牙卵泡细胞(DFCs)是牙周炎细胞疗法的天然来源。牙周炎被口腔病原体如革兰氏阴性细菌牙龈卟啉单胞菌感染后开始。脂多糖(LPS)是革兰氏阴性细菌外膜的主要成分。先前的研究表明,特别是牙龈卟啉单胞菌LPS诱导PDL细胞中促炎性细胞因子的表达,并干扰牙干细胞的分化。我们的研究首次调查了对DFC的LPS管理。材料和方法:我们评估了在P存在下细胞的增殖(WST1分析),细胞因子IL1β,IL8和IL6的表达(实时RT-PCR)以及DFC的成骨分化(ALP活性和茜素红染色)。牙龈脂多糖和大肠杆菌脂多糖。结果:大肠杆菌LPS处理后,所有测试的促炎细胞因子均大大增加。牙龈卟啉单胞菌LPS仅诱导IL8的表达,但该表达明显低于大肠杆菌LPS施用后的表达。施用大肠杆菌LPS后,DFC中的ALP活性显着高于施用牙龈卟啉单胞菌LPS后或在正常细胞分化条件下的DLP中。但是,LPS抑制了两种细菌的​​矿化作用。结论:LPS干扰DFC中的成骨分化。而且,在施用牙龈卟啉单胞菌LPS后,DFC中诱导促炎性细胞因子的失败与PDL成纤维细胞的失败大不相同。对于DFC的牙周炎的细胞疗法,必须考虑DFC的这些免疫学特性。

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