The human periodontal ligament cell: a fibroblast-like cell acting as an immune cell

Jönsson, Daniel; Nebel, Daniel; Bratthall, Gunilla; Nilsson, Bengt‐Olof

doi:10.1111/j.1600-0765.2010.01331.x

Cited by 141 publications

(133 citation statements)

References 37 publications

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“…Also, it is reasonable to suggest that periodontal ligament cells play a key role as promoters of periodontal inflammation through these mechanisms 9) . Since a recent study suggested that periodontal ligament cells may have important implications for the development of new therapeutic strategies to treat periodontitis 10) .…”

Section: Introductionmentioning

confidence: 99%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and PGE2 and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and PGE2 release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

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Section: Introductionmentioning

confidence: 99%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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“…Along with various other cell types of periodontium, hPdLCs may be involved in the host response to periodontitis [19]. hPdLCs respond to P. gingivalis or its components by initiating an inflammatory response, including the expression and production of proinflammatory cytokines and chemokines, as shown both at the mRNA and protein levels [20]–[22].…”

Section: Introductionmentioning

confidence: 99%

Endocannabinoids and Inflammatory Response in Periodontal Ligament Cells

et al. 2014

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Endocannabinoids are associated with multiple regulatory functions in several tissues. The main endocannabinoids, anandamide (AEA) and 2-arachidonylglycerol (2-AG), have been detected in the gingival crevicular fluid of periodontitis patients, but the association between periodontal disease or human periodontal ligament cells (hPdLCs) and endocannabinoids still remain unclear. The aim of the present study was to examine the effects of AEA and 2-AG on the proliferation/viability and cytokine/chemokine production of hPdLCs in the presence/absence of Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS). The proliferation/viability of hPdLCs was measured using 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide (MTT)-assay. Interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemotactic protein-1 (MCP-1) levels were examined at gene expression and protein level by real-time PCR and ELISA, respectively. AEA and 2-AG did not reveal any significant effects on proliferation/viability of hPdLCs in the absence of P. gingivalis LPS. However, hPdLCs viability was significantly increased by 10–20 µM AEA in the presence of P. gingivalis LPS (1 µg/ml). In the absence of P. gingivalis LPS, AEA and 2-AG did not exhibit any significant effect on the expression of IL-8 and MCP-1 expression in hPdLCs, whereas IL-6 expression was slightly enhanced by 10 µM 2-AG and not affected by AEA. In P.gingivalis LPS stimulated hPdLCs, 10 µM AEA down-regulated gene-expression and protein production of IL-6, IL-8, and MCP-1. In contrast, 10 µM 2-AG had an opposite effect and induced a significant up-regulation of gene and protein expression of IL-6 and IL-8 (P<0.05) as well as gene-expression of MCP-1 in P. gingivalis LPS stimulated hPdLCs. Our data suggest that AEA appears to have an anti-inflammatory and immune suppressive effect on hPdLCs’ host response to P.gingivalis LPS, whereas 2-AG appears to promote detrimental inflammatory processes. In conclusion, AEA and 2-AG might play an important role in the modulation of periodontal inflammation.

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“…Periodontal ligament (PDL) links teeth to alveolar bone and participates in alveolar bone remodeling. PDL cells reside in PDL space, characterized by the production of collagen fibers and mineralized tissue (Jonsson et al, 2011). Pattern recognition receptors (PRRs) on the resident cells of the periodontium play an important role in the innate immune response by recognizing bacteria-derived factors and promoting the production of cytokines and chemokines, which are key mediators of inflammation and bone loss (Cochran, 2008;Di Benedetto et al, 2013).…”

mentioning

confidence: 99%

S100A9-induced release of interleukin (IL)-6 and IL-8 through toll-like receptor 4 (TLR4) in human periodontal ligament cells

Gao

Xin

Zheng

et al. 2015

Molecular Immunology

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The human periodontal ligament cell: a fibroblast-like cell acting as an immune cell

Abstract: Therefore, pharmacological treatment of periodontitis should aim to reduce the release of proinflammatory agents not only from classical inflammatory cells but also from periodontal ligament cells.

Cited by 141 publications

References 37 publications

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Endocannabinoids and Inflammatory Response in Periodontal Ligament Cells

S100A9-induced release of interleukin (IL)-6 and IL-8 through toll-like receptor 4 (TLR4) in human periodontal ligament cells

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