Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; College of Stomatology, Shanghai Jiao Tong University, Shanghai, China; National Center for Stomatology, Shanghai, China; National Clinical Research Center for Oral Diseases, Shanghai, China; Shanghai Key Laboratory of Stomatology, Shanghai, China; Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital Research Center, Shanghai Jiao Tong University, Shanghai, China.
Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; College of Stomatology, Shanghai Jiao Tong University, Shanghai, China; National Center for Stomatology, Shanghai, China; National Clinical Research Center for Oral Diseases, Shanghai, China; Shanghai Key Laboratory of Stomatology, Shanghai, China; Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital Research Center, Shanghai Jiao Tong University, Shanghai, China.
Arch Oral Biol. 2021 Sep;129:105161. doi: 10.1016/j.archoralbio.2021.105161. Epub 2021 May 19.
The overall aim of this research was to investigate the differences in the expression of programmed death ligand 1 (PD-L1) in human gingival fibroblasts (HGFs) between a periodontal healthy group and a periodontal inflammatory group. and explore the possible mechanism involved.
Differences in PD-L1 mRNA and protein expression in HGFs from a periodontal healthy group and a periodontal inflammatory group were examined by qPCR and western blotting, respectively, and were further tested after lipopolysaccharide (LPS) stimulation in both groups. The effects of a p38 pathway inhibitor on the changes in p38 phosphorylation levels and PD-L1 expression after LPS stimulation were investigated in both groups.
PD-L1 mRNA and protein levels in HGFs in the periodontal inflammatory group were significantly higher than those in the periodontal healthy group (p < 0.05). After 10 μg/mL LPS stimulation, PD-L1 mRNA levels in HGFs from both groups increased significantly (p < 0.05), peaking at 4 h, and the peak was significantly higher in the periodontal inflammatory group than in the periodontal healthy group (p < 0.05). However, PD-L1 protein expression was upregulated only in the inflammatory group (p < 0.05). Inhibition of the p38 pathway in HGFs decreased p38 phosphorylation in both groups (p < 0.05) but this treatment reversed the LPS-induced increase in PD-L1 mRNA and protein levels only in the inflammatory group (p < 0.05).
In the periodontal inflammatory state, the expression of PD-L1 in HGFs is more easily activated, and may be influenced by the p38 pathway.
本研究的总体目的是研究牙周健康组和牙周炎症组人牙龈成纤维细胞（HGF）中程序性死亡配体 1（PD-L1）表达的差异，并探讨其可能的机制。
通过 qPCR 和 Western blot 分别检测牙周健康组和牙周炎症组 HGF 中 PD-L1 mRNA 和蛋白表达的差异，并进一步检测两组 LPS 刺激后的变化。研究 p38 通路抑制剂对 LPS 刺激后两组 p38 磷酸化水平和 PD-L1 表达变化的影响。
牙周炎症组 HGF 中 PD-L1 mRNA 和蛋白水平明显高于牙周健康组（p<0.05）。经 10μg/mL LPS 刺激后，两组 HGF 中 PD-L1 mRNA 水平均明显升高（p<0.05），4 h 时达峰值，牙周炎症组明显高于牙周健康组（p<0.05）。然而，只有炎症组的 PD-L1 蛋白表达上调（p<0.05）。HGF 中 p38 通路的抑制降低了两组的 p38 磷酸化（p<0.05），但这种治疗仅在炎症组逆转了 LPS 诱导的 PD-L1 mRNA 和蛋白水平的增加（p<0.05）。
在牙周炎症状态下，HGF 中 PD-L1 的表达更容易被激活，并且可能受到 p38 通路的影响。
