Historical aspects of studies on roles of the inflammasome in the pathogenesis of periodontal diseases

Summary

The proinflammatory cytokine interleukin (IL)-1β is produced as inactive pro-IL-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- 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 Bostanci et al. suggested the involvement of inflammasomes in periodontal disease 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 that 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 also been accumulated that the inflammasome activation is modulated by the periodontopathic bacteria other than P. gingivalis.

Thus, 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.

This article is protected by copyright. All rights reserved.

http://ift.tt/2rCA7xx