Following the infection of the periodontal pathogen, namely P. gingivalis, it was found that the release of IL-1β, IL-6, and IL-18; the gene expression of pro-IL-1β and pro-IL-18; and the activity of caspase-1 in wild-type mice were significantly enhanced in comparison to NLRP3-deficient mice [90]. Here, IL1B is linked to infection.