New strategy based on the organogenesis signal control for periodontal disease

与健康对照组织相比，慢性牙周炎组织中Wnt5a mRNA表达上调。P. gingivalis LPS诱导THP-1单核细胞Wnt5a mRNA表达，在刺激后4小时达到峰值。P. gingivalis LPS诱导Wnt5a mRNA的上调高于大肠杆菌LPS。LPS受体TLR2和TLR4在THP-1细胞表面均有表达。P. gingivalis LPS诱导IkBa降解，并能提高NF-kB与DNA的结合活性。NF-kB抑制剂可抑制牙龈假单胞菌lps诱导的Wnt5a表达，提示NF-kB参与其中。此外，IFN-g协同增强了P. gingivalis lps诱导的Wnt5a的产生。药理研究和siRNA实验表明，STAT1在牙龈卟噬菌lps诱导的Wnt5a表达中起重要作用。这些结果表明，牙龈假单胞菌对Wnt5a表达的调节可能在牙周炎症过程中发挥重要作用，并为开发新的治疗方法提供了靶点。

Wnt5a mRNA expression was up-regulated in chronic periodontitis tissue as compared to healthy control tissue. P. gingivalis LPS induced Wnt5a mRNA in the human monocytic cell line THP-1 with a peak at 4 hrs after stimulation. P. gingivalis LPS induced higher up-regulation of Wnt5a mRNA than E. coli LPS. The LPS receptors TLR2 and TLR4 were equally expressed on the surface of THP-1 cells. P. gingivalis LPS induced IkBa degradation and was able to increase the NF-kB binding activity to DNA. P. gingivalis LPS-induced Wnt5a expression was inhibited by NF-kB inhibitors, suggesting NF-kB involvement. Furthermore, IFN-g synergistically enhanced the P. gingivalis LPS-induced production of Wnt5a. Pharmacological investigation and siRNA experiments showed that STAT1 was important for P. gingivalis LPS-induced Wnt5a expression. These results suggest that the modulation of Wnt5a expression by P. gingivalis may play an important role in the periodontal inflammatory process and serve a target for the development of new therapies.