Department of Oral Molecular Microbiology, Faculty of Dental Medicine and Graduate School of Dental Medicine, Hokkaido University, Hokkaido, Japan.
Mol Oral Microbiol. 2018 Jun;33(3):203-211. doi: 10.1111/omi.12217. Epub 2018 Feb 20.
The proinflammatory cytokine interleukin-1β (IL-1β) is produced as inactive proIL-1β and then processed by caspase-1 to become active. In 2002, it was demonstrated that the intracellular multiprotein complex known as the inflammasome functions as a molecular platform to trigger activation of caspase-1. Inflammasomes are known to function as intracellular sensors for a broad spectrum of various pathogen-associated and damage-associated molecular patterns. In 1985, it was demonstrated that Porphyromonas gingivalis, a representative bacterium causing chronic periodontitis, induces IL-1 production by murine peritoneal macrophages. Since then, many studies have suggested that IL-1, particularly IL-1β plays key roles in the pathogenesis of periodontal diseases. However, the term "inflammasome" was not used until the involvement of inflammasomes in periodontal disease was suggested in 2009. Several subsequent studies on the roles of the inflammasome in the pathogenesis of periodontal diseases have been published. Interestingly, two contradictory reports on the modulation of inflammasomes by P. gingivalis have been published. Some papers have described how P. gingivalis activates the inflammasome to produce IL-1β whereas some stated that P. gingivalis inhibits inflammasome activation to subvert immune responses. Several lines of evidence have suggested that the inflammasome activation is modulated by periodontopathic bacteria other than P. gingivalis. Hence, studies on the roles of inflammasomes in the pathogenesis of periodontal diseases began only 8 years ago and many pathological roles of inflammasomes remain to be clarified.
促炎细胞因子白细胞介素-1β（IL-1β）以前体形式(proIL-1β)合成，然后被半胱天冬酶-1(caspase-1)加工成有活性的形式。2002 年，研究表明细胞内多蛋白复合物，即被称为炎症小体（inflammasome），作为一种分子平台，触发 caspase-1 的激活。炎症小体被认为是细胞内识别多种病原体相关和损伤相关分子模式的传感器。1985 年，研究表明牙龈卟啉单胞菌（Porphyromonas gingivalis），一种引起慢性牙周炎的代表性细菌，可诱导鼠腹腔巨噬细胞产生 IL-1。此后，许多研究表明，IL-1，特别是 IL-1β，在牙周病的发病机制中发挥关键作用。然而，直到 2009 年，炎症小体被认为与牙周病有关时，才开始使用“炎症小体”一词。随后发表了几项关于炎症小体在牙周病发病机制中的作用的研究。有趣的是，关于牙龈卟啉单胞菌对炎症小体的调节有两个相互矛盾的报告。一些论文描述了牙龈卟啉单胞菌如何激活炎症小体产生 IL-1β，而另一些则指出牙龈卟啉单胞菌抑制炎症小体的激活以颠覆免疫反应。有几条证据表明，除了牙龈卟啉单胞菌之外，其他牙周病病原体也可以调节炎症小体的激活。因此，关于炎症小体在牙周病发病机制中的作用的研究仅在 8 年前开始，炎症小体的许多病理作用仍有待阐明。
