Regulation of the NLRP3 inflammasome in Porphyromonas gingivalis-accelerated periodontal disease

Objective Porphyromonas gingivalis is involved in the pathogenesis of chronic inflammatory periodontal disease. Recent studies have suggested that the NLRP3 inflammasome plays an important role in the development of chronic inflammation. We investigated a possible association between the inflammasom...

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Bibliographic Details
Published in:Inflammation research 2017-01, Vol.66 (1), p.59-65
Main Authors: Yamaguchi, Yohei, Kurita-Ochiai, Tomoko, Kobayashi, Ryoki, Suzuki, Toshihiko, Ando, Tomohiro
Format: Article
Language:English
Subjects:
Allergology
Alveolar Bone Loss - metabolism
Animals
Biomedical and Life Sciences
Biomedicine
Bone and Bones - drug effects
Bone and Bones - metabolism
Cytokines - genetics
Cytokines - metabolism
Dermatology
Gingiva - metabolism
Immunology
Inflammasomes - genetics
Inflammasomes - metabolism
Macrophages, Peritoneal - metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Neurology
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
Original Research Paper
Osteoprotegerin - genetics
Periodontal Diseases - metabolism
Pharmacology/Toxicology
Porphyromonas gingivalis
RANK Ligand - genetics
Rheumatology
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Summary:Objective Porphyromonas gingivalis is involved in the pathogenesis of chronic inflammatory periodontal disease. Recent studies have suggested that the NLRP3 inflammasome plays an important role in the development of chronic inflammation. We investigated a possible association between the inflammasome in gingival inflammation and bone loss induced by P. gingivalis infection using NLRP3-deficient mice. Methods Wild-type and NLRP3-deficient mice were injected orally with P. gingivalis . We assessed alveolar bone loss, expression of pro-interleukin (IL)-1β, pro-IL-18, receptor activator of nuclear factor kappa-B ligand (RANKL), and osteoprotegerin (OPG) in gingival tissue, as well as IL-1β, IL-18, and IL-6 production and caspase-1 activity in peritoneal macrophages. Results Porphyromonas gingivalis challenge significantly increased alveolar bone loss; gingival gene expression of pro-IL-1β, pro-IL-18, and RANKL; production of IL-1β, IL-18, and IL-6; and caspase-1 activity in peritoneal macrophages of wild-type mice, but did not affect NLRP3-deficient mice. Meanwhile, OPG mRNA expression in gingival tissue and peritoneal IL-6 production were significantly higher in NLRP3-knockout mice. Conclusions Porphyromonas gingivalis activated innate immune cells via the NLRP3 inflammasome. These results suggest that the NLRP3 inflammasome, followed by a response from the IL-1 family, is critical in periodontal disease induced by wild-type P. gingivalis challenge via sustained inflammation.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-016-0992-4