Objectives: This study aimed to clarify the regulatory role of Th17-Treg balance in periodontitis and further reveal Treg plasticity.
Materials and methods: An experimental periodontitis model was established by ligation and injection of Pg-LPS. Inflammatory factors were measured by ELISA and RT-PCR. Alveolar bone absorption was evaluated by micro-CT and histomorphology. Quantities of Treg and Th17 cell and their related gene expression were examined. Furthermore, after magnetic bead-sorting spleen Treg cells, Treg/Th17 characteristic genes were explored. Immunofluorescence double staining of Foxp3 and IL-17 was conducted to further reveal Treg plasticity.
Results: Inflammatory cytokines in serum and gingival tissue increased significantly in periodontitis, which revealed obvious crestal bone loss. Further analysis showed that the number of Th17 cells and expression of related genes increased more significantly than Treg cells, demonstrating Treg-Th17 imbalance. Flow cytometry showed that the proportions of Treg cells in the blood and spleen were lower in periodontitis group. Furthermore, Foxp3 was downregulated, and Rorc/ IL-17A were increased in Treg cells of periodontitis group. Immunofluorescence double staining showed significantly increased number of IL-17+Foxp3+ cells in periodontitis.
Conclusions: These results provided evidence that Treg cells showed characteristics of Th17 cells in mice with periodontitis, although its mechanisms require further study.
Keywords: CD4+ T cells; Treg plasticity; Treg-Th17 imbalance; chronic periodontitis.
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