NanoGlycobiology Research Group, Institute of Biochemistry, Department of Chemistry, Universität für Bodenkultur Wien, Vienna, Austria.
NanoGlycobiology Research Group, Institute of Biochemistry, Department of Chemistry, Universität für Bodenkultur Wien, Vienna, Austria.
Arch Oral Biol. 2024 Aug;164:106004. doi: 10.1016/j.archoralbio.2024.106004. Epub 2024 May 16.
The red-complex bacteria Porphyromonas gingivalis and Tannerella forsythia together with Fusobacterium nucleatum are essential players in periodontitis. This study investigated the bacterial interplay with human periodontal ligament mesenchymal stromal cells (hPDL-MSCs) which act in the acute phase of periodontal infection.
The capability of the bacteria to induce an inflammatory response as well as their viability, cellular adhesion and invasion were analyzed upon mono- and co-infections of hPDL-MSCs to delineate potential synergistic or antagonistic effects. The expression level and concentration of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein (MCP)-1 were measured using qRT-PCR and ELISA. Viability, invasion, and adhesion were determined quantitatively using agar plate culture and qualitatively by confocal microscopy.
Viability of P. gingivalis and T. forsythia but not F. nucleatum was preserved in the presence of hPDL-MSCs, even in an oxygenated environment. F. nucleatum significantly increased the expression and concentration of IL-6, IL-8 and MCP-1 in hPDL-MSCs, while T. forsythia and P. gingivalis caused only a minimal inflammatory response. Co-infections in different combinations had no effect on the inflammatory response. Moreover, P. gingivalis mitigated the increase in cytokine levels elicited by F. nucleatum. Both red-complex bacteria adhered to and invaded hPDL-MSCs in greater numbers than F. nucleatum, with only a minor effect of co-infections.
Oral bacteria of different pathogenicity status interact differently with hPDL-MSCs. The data support P. gingivalis' capability to manipulate the inflammatory host response. Further research is necessary to obtain a comprehensive picture of the role of hPDL-MSCs in more complex oral biofilms.
红色复合体细菌牙龈卟啉单胞菌和福赛斯坦纳菌与核梭杆菌一起是牙周炎的重要参与者。本研究调查了细菌与人牙周膜间充质基质细胞(hPDL-MSCs)的相互作用,这些细胞在牙周感染的急性期发挥作用。
分析了细菌在单感染和共感染 hPDL-MSCs 时诱导炎症反应的能力,以及其活力、细胞黏附和侵袭能力,以描绘潜在的协同或拮抗作用。使用 qRT-PCR 和 ELISA 测量白细胞介素(IL)-6、IL-8 和单核细胞趋化蛋白(MCP)-1 的表达水平和浓度。使用琼脂平板培养和共聚焦显微镜定性地定量测定活力、侵袭和黏附。
即使在有氧环境中,hPDL-MSCs 存在时,牙龈卟啉单胞菌和福赛斯坦纳菌的活力得以维持,而核梭杆菌的活力则没有。核梭杆菌显著增加了 hPDL-MSCs 中 IL-6、IL-8 和 MCP-1 的表达和浓度,而福赛斯坦纳菌和牙龈卟啉单胞菌仅引起轻微的炎症反应。不同组合的共感染对炎症反应没有影响。此外,牙龈卟啉单胞菌减轻了核梭杆菌引起的细胞因子水平的增加。红色复合体细菌比核梭杆菌更能黏附和侵袭 hPDL-MSCs,共感染的影响较小。
不同致病性状态的口腔细菌与 hPDL-MSCs 相互作用方式不同。数据支持牙龈卟啉单胞菌操纵炎症宿主反应的能力。需要进一步研究以获得 hPDL-MSCs 在更复杂口腔生物膜中作用的全面图景。