Increased levels of interleukin-33 in gingival crevicular fluids of patients with chronic periodontitis

Sağlam, Mehmet; Köseoğlu, Serhat; Aral, Cüneyt Asım; Savran, Levent; Pekbağrıyanık, Tuğba; Cetinkaya, Ayse

doi:10.1007/s10266-016-0259-0

Cited by 24 publications

(22 citation statements)

References 30 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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“…In human, high IL-33 overexpression was recorded in the gingiva of patients affected by CP and may act as a triggering factor for the recruitment of B and T lymphocytes expressing RANK-L [20]. But in gingival crevicular fluid (an inflammatory exudate collected in the periodontal pocket) conflicting results regarding IL-33 levels have been reported in patients affected by CP [21–23]. Interestingly, Pg has been described to upregulate IL-33 mRNA expression in gingival epithelial cells through the PAR-2 signaling pathway [24].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis

Lapérine

Cloître

Caillon³

et al. 2016

PLoS ONE

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IntroductionChronic Periodontitis (CP) is an inflammatory disease of bacterial origin that results in alveolar bone destruction. Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP. It has been suggested that IL-33, could be of interest in CP.Objectivethe present study aims to analyze whether and how IL-33 and RANK-L and/or their interplay are involved in the bone destruction associated to CP.Material and MethodsmRNAs and protein expressions of IL-33 and RANK-L were analyzed in healthy and CP human gingival samples by immunohistochemistry (IHC) and RT-qPCR. Murine experimental periodontitis (EP) was induced using Pg infected ligature and Pg free ligature around the first maxillary molar. Alveolar bone loss was recorded by μCT. Mouse gingival explants were stimulated for 24 hours with IL-33 and RANK-L mRNA expression investigated by RT-qPCR. Human oral epithelial cells were infected by Pg for 6, 12; 24 hours and IL-33 and RANK-L mRNA expressions were analyzed by RT-qPCR.ResultsIL-33 is overexpressed in gingival epithelial cells in human affected by CP as in the murine EP. In human as in murine gingival cells, RANK-L was independently induced by Pg and IL-33. We also showed that the Pg-dependent RANK-L expression in gingival epithelial cells occured earlier than that of IL-33.ConclusionOur results evidence that IL-33 overexpression in gingival epithelial cells is associated with CP and may trigger RANK-L expression in addition to a direct effect of Pg. Finally, IL-33 may act as an extracellular alarmin (danger signal) showing proinflammatory properties in CP perpetuating bone resorption induced by Pg infection.

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“…[ 21 ] In contrast, a different survey suggested that crevicular fluid was elevated in individuals with gingivitis and chronic periodontitis compared to unaffected individuals, and that IL-33 levels in crevicular fluid were significantly lower in patients with chronic periodontitis than in patients with gingivitis and patients without periodontal disease. [ 23 ] Similarly, in another study, IL-33 activity was found to be associated with RANKL-dependent bone resorption, and thus with chronic periodontal disease. [ 26 ]…”

Section: Discussionmentioning

confidence: 86%

Association between pro-inflammatory cytokine interleukin-33 and periodontal disease in the elderly: A retrospective study

Rodrigues

Miguel

Mendes

et al. 2017

J Indian Soc Periodontol

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Background:Senescence is a multifactorial process that in humans may be accompanied by inflammation and immune dysfunction in the oral cavity. Notably, periodontal disease, considered one of the most common inflammatory disorders in the oral cavity, has also been linked to the onset of other chronic inflammatory diseases common in the elderly. Thus, investigating immunity and inflammation during senescence may not only illuminate the pathophysiology of periodontal disease, but also identify new therapeutic targets.Materials and Methods:To this end, we retrospectively and systematically reviewed studies of immune molecules associated with periodontal disease. These studies were identified in PubMed from three independent searches based on distinct sets of search terms.Results:The data highlight the need to further investigate inflammatory molecules involved in chronic periodontal disease in the elderly, but strongly suggest that interleukin (IL)-33 is involved. Indeed, various genetic and environmental factors appear to contribute to pathogenesis via IL-33.Conclusion:The IL-33 axis may be promising therapeutic target in elderly patients.

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Increased levels of interleukin-33 in gingival crevicular fluids of patients with chronic periodontitis

Cited by 24 publications

References 30 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

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis

Association between pro-inflammatory cytokine interleukin-33 and periodontal disease in the elderly: A retrospective study

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