Possible Roles of IL-33 in Periodontal Diseases: Porphyromonas gingivalis Induced IL-33 in Human Gingival Epithelial Cells

Tada, Hiroyuki; Shimauchi, Hidetoshi; Takada, Haruhiko; Matsushita, Kazunobu

doi:10.1007/978-4-431-55192-8_25

Cited by 2 publications

(2 citation statements)

References 34 publications

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“…The presence of IL‐33 within the oral tissues was recently demonstrated. While periodontal pathogenic bacteria Porphyromonas gingivalis strongly stimulated IL‐33 mRNA expression in gingival epithelial cells, IL‐33 expression is elevated in the inflamed gingival crevicular fluid and gingival epithelium of chronic periodontitis patients . Association of increased IL‐33 level with periodontitis and alveolar bone resorption and loss was also reported .…”

Section: Introductionmentioning

confidence: 93%

IL‐33 guides osteogenesis and increases proliferation and pluripotency marker expression in dental stem cells

et al. 2018

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Objectives Soluble IL‐33 (interleukin (IL)‐1‐like cytokine) acts as endogenous alarm signal (alarmin). Since alarmins, besides activating immune system, act to restore tissue homeostasis, we investigated whether IL‐33 exerts beneficial effects on oral stem cell pull. Materials and Methods Clonogenicity, proliferation, differentiation and senescence of stem cells derived from human periodontal ligament (PDLSCs) and dental pulp (DPSCs) were determined after in vitro exposure to IL‐33. Cellular changes were detected by flow cytometry, Western blot, immunocytochemistry and semiquantitative RT‐PCR. Results IL‐33 stimulated proliferation, clonogenicity and expression of pluripotency markers, OCT‐4, SOX‐2 and NANOG, but it inhibited ALP activity and mineralization in both PDLSCs and DPSCs. Higher Ki67 expression and reduced β‐galactosidase activity in IL‐33‐treated cells were demonstrated, whereas these trends were more conspicuous in osteogenic medium. However, after 7‐day IL‐33 pretreatment, differentiation capacity of IL‐33‐pretreated cells was retained, and increased ALP activity was observed in both cell types. Results showed that IL‐33 regulates NF‐κB and β‐catenin signalling, indicating the association of these molecules with changes observed in IL‐33‐treated PDLSCs and DPSCs, particularly their proliferation, pluripotency‐associated marker expression and osteogenesis. Conclusions IL‐33 treatment impairs osteogenesis of PDLSCs and DPSCs, while increases their clonogenicity, proliferation and pluripotency marker expression. After exposure to IL‐33, osteogenic capacity of cells stayed intact. NF‐κB and β‐catenin are implicated in the effects achieved by IL‐33 in PDLSCs and DPSCs.

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Section: Introductionmentioning

confidence: 93%

IL‐33 guides osteogenesis and increases proliferation and pluripotency marker expression in dental stem cells

et al. 2018

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“…gingivalis invades gingival epithelial cells [ 27 ]. We recently discussed a possible role of IL-33 in the pathogenesis of chronic periodontitis [ 28 ]. Although gingival tissues from patients with chronic periodontitis express IL-33 [ 29 ], whether or not P .…”

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells

et al. 2016

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The cytokine IL-33 is constitutively expressed in epithelial cells and it augments Th2 cytokine-mediated inflammatory responses by regulating innate immune cells. We aimed to determine the role of the periodontal pathogen, Porphyromonas gingivalis, in the enhanced expression of IL-33 in human gingival epithelial cells. We detected IL-33 in inflamed gingival epithelium from patients with chronic periodontitis, and found that P. gingivalis increased IL-33 expression in the cytoplasm of human gingival epithelial cells in vitro. In contrast, lipopolysaccharide, lipopeptide, and fimbriae derived from P. gingivalis did not increase IL-33 expression. Specific inhibitors of P. gingivalis proteases (gingipains) suppressed IL-33 mRNA induction by P. gingivalis and the P. gingivalis gingipain-null mutant KDP136 did not induce IL-33 expression. A small interfering RNA for protease-activated receptor-2 (PAR-2) as well as inhibitors of phospholipase C, p38 and NF-κB inhibited the expression of IL-33 induced by P. gingivalis. These results indicate that the PAR-2/IL-33 axis is promoted by P. gingivalis infection in human gingival epithelial cells through a gingipain-dependent mechanism.

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Possible Roles of IL-33 in Periodontal Diseases: Porphyromonas gingivalis Induced IL-33 in Human Gingival Epithelial Cells

Cited by 2 publications

References 34 publications

IL‐33 guides osteogenesis and increases proliferation and pluripotency marker expression in dental stem cells

IL‐33 guides osteogenesis and increases proliferation and pluripotency marker expression in dental stem cells

Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells

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