[Expression and significance of Treg/Th17 and CD4+/CD8+ T lymphocytes in experimental periodontitis in rats].

To explore the expression of helper T cell 17/regulatory T cell (Th17/Treg) and CD4+/CD8+ T lymphocyte in experimental periodontitis in rats, and analyze its clinical significance.Twenty SPF male SD rats were randomly divided into experimental group (inoculate Porphyromonas gingivalis suspension into gingival sulcus) and control group, with 10 rats in each group. The experimental group was smeared with Porphyromonas gingivalis suspension every other day within 1 week after operation, and the two groups were caged for 8 weeks. After the rats were sacrifical under anesthesia, the jaw tissue of the left maxillary second molar was stained with methylene blue to observe and measure the loss of alveolar bone (ABL). Hematoxylin-eosin (H-E) staining was used to observe the histopathological changes of the jaw. Rat peripheral blood mononuclear cells (PBMC) and T cells were isolated and cultured, Treg, Th17 cells and CD4+, CD8+ T lymphocytes in peripheral blood were detected by flow cytometry. The levels of serum interleukin-17(IL-17), IL-10 and IL-4, INF-γ were detected by enzyme-linked immunosorbent assay (ELISA). Expression changes of retinoic acid related orphan nuclear receptor (RORγt), forkhead wing like transcription factor 3 (Foxp3) and gap junction protein(Cx40) in jaw tissue were detected by Western blot. The data were statistically analyzed by SPSS 19.0 software package.Compared with the control group, ABL, peripheral blood Th17 ratio, Th17/Treg ratio, CD4+ ratio, CD4+/CD8+ T lymphocyte ratio, serum IL-17, IL-10 and IL-4 level, Foxp3 and Cx40 protein in jaw tissue were signifinantly increased in the experimental group(P<0.05), while Treg ratio, INF-γ, RORγt protein in jaw tissue significantly decreased(P<0.05) in the experimental group.Imbalance of Treg/Th17 and CD4+/CD8+ T lymphocytes leads to the abnormal high expression of inflammatory factors IL-17, IL-10 and IL-4, which may be closely related to the pathogenesis of experimental periodontitis.