{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T23:34:51Z","timestamp":1771457691160,"version":"3.50.1"},"reference-count":84,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,2,20]],"date-time":"2018-02-20T00:00:00Z","timestamp":1519084800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Oral Microbiology"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The proinflammatory cytokine interleukin\u20101\u03b2 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2) is produced as inactive pro<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 and then processed by caspase\u20101 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\u20101. Inflammasomes are known to function as intracellular sensors for a broad spectrum of various pathogen\u2010associated and damage\u2010associated molecular patterns. In 1985, it was demonstrated that <jats:italic>Porphyromonas gingivalis<\/jats:italic>, a representative bacterium causing chronic periodontitis, induces <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 production by murine peritoneal macrophages. Since then, many studies have suggested that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101, particularly <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 plays key roles in the pathogenesis of periodontal diseases. However, the term \u201cinflammasome\u201d 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 <jats:italic>P.\u00a0gingivalis<\/jats:italic> have been published. Some papers have described how <jats:italic>P.\u00a0gingivalis<\/jats:italic> activates the inflammasome to produce <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 whereas some stated that <jats:italic>P.\u00a0gingivalis<\/jats:italic> inhibits inflammasome activation to subvert immune responses. Several lines of evidence have suggested that the inflammasome activation is modulated by periodontopathic bacteria other than <jats:italic>P.\u00a0gingivalis<\/jats:italic>. Hence, studies on the roles of inflammasomes in the pathogenesis of periodontal diseases began only 8\u00a0years ago and many pathological roles of inflammasomes remain to be clarified.<\/jats:p>","DOI":"10.1111\/omi.12217","type":"journal-article","created":{"date-parts":[[2018,1,23]],"date-time":"2018-01-23T14:16:58Z","timestamp":1516717018000},"page":"203-211","source":"Crossref","is-referenced-by-count":37,"title":["Historical aspects of studies on roles of the inflammasome in the pathogenesis of periodontal diseases"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6497-9073","authenticated-orcid":false,"given":"K.","family":"Shibata","sequence":"first","affiliation":[{"name":"Department of Oral Molecular Microbiology Faculty of Dental Medicine and Graduate School of Dental Medicine Hokkaido University  Hokkaido 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