Purpose: To study the temporal expression of programmed death receptor 1 (PD-1) and its ligand (PD-L1) in the development of periodontitis in rats.
Methods: SD rats were randomly divided into control group and model group, and 4 subgroups were divided in each model group according to the time of measurement: group A (1 week), group B (2 weeks), group C (3 weeks) and group D (4 weeks). There were 8 rats in each subgroup. Maxillary periodontitis models were made by using "thread ligation + vaccination LPS-PG" in rats. Periodontal tissue specimens were examined and bone resorption areas were determined in each group. Tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1β), interleukin 6 (IL-6) and transforming growth factor beta (TGF-β) mRNA in periodontal tissue in each group were determined by RT-PCR method. PD-1 and PD-L1 protein expression in periodontal tissues in each group were determined by Western blotting. The data were analyzed by SPSS 22.0 software package.
Results: During modeling period, amelocemental junction-alveolar crest(ACJ-AC) distance and bone resorption area of the first molar in model group gradually increased (P<0.05), which were significantly different from the control group at the corresponding time point (P<0.01). During modeling period, TNF-α, IL-1β and IL-6 mRNA level in periodontal tissues in the model group was continuously increased(P<0.05), and TGF-β mRNA was continuously decreased(P<0.05), which was significantly different from the control group at the corresponding time point(P<0.01). During disease progress, PD-1 and PD-L1 protein level in periodontal tissues in each model group was continuously increased(P<0.05), which was significantly different from the control group at the corresponding time point (P<0.01); and PD-1 and PD-L1 protein levels in periodontal tissues in each model group was positively correlated to TNF-α and IL-6 mRNA levels(P<0.01).
Conclusions: PD-1, as an immunosuppressive molecule and its receptor PD-L1, can promote the progression of periodontal inflammation, and its effect may be achieved by regulating the expression of TNF-α and IL-6.Regulating the expression of PD-1 and PD-L1 may be a new target for the treatment of periodontitis.
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