Analysis of regulatory mechanism of bone destruction and inflammation in experimental periodontitis mediated by IL-27 receptor

WSX-1基因是IL-27受体的一个亚基，参与免疫和炎症的调节。我们使用WSX-1基因敲除小鼠分析了IL-27在牙周炎骨破坏中的作用。牙龈卟啉单胞菌是引起牙周炎的主要病原菌之一。与野生型小鼠相比，WSX-1 KO小鼠中牙龈卟啉单胞菌引起的牙槽骨丢失增加。牙周炎小鼠脾脏中CD 4 + T细胞产生IL-17的量增加，WSX-1 KO小鼠IFN-γ和IL-17的产生进一步增加。牙龈卟啉单胞菌感染促进巨噬细胞向破骨细胞分化，并且感染诱导的破骨细胞形成在WSX-1 KO小鼠的巨噬细胞中增强。提示IL-27受体信号通过直接或间接影响破骨细胞的生成，参与牙周炎的骨丢失。

WSX-1 gene is a subunit of receptor for IL-27 which is involved in the regulation of immunity and inflammation. We analyzed the role of IL-27 in bone destruction of periodontitis using WSX-1 knocked-out mice. Mice were infected with Porphyromonas gingivalis which is one of major pathogens in periodontitis. Alveolar bone loss following P. gingivalis was enhanced in WSX-1 KO mice compared to those in wild-type mice. CD4-positive T cells in spleen of periodontitis mice produced higher amount of IL-17, and the production of IFN-γand IL-17 was further promoted in WSX-1 KO mice. P. gingivalis infection promoted differentiation from macrophages into osteoclasts, and osteoclast formation induced by infection was enhanced in macrophage of WSX-1 KO mice. The data suggest that signals through IL-27 receptor are involved in bone loss of periodontitis by affecting osteoclastogenesis directly and indirectly.