Porphyromonas gingivalis induces RANKL in bone marrow stromal cells: Involvement of the p38 MAPK

Reddi, Durga; Brown, Stuart J.; Belibasakis, Georgios N.

doi:10.1016/j.micpath.2011.09.001

Cited by 13 publications

(18 citation statements)

References 35 publications

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“…Recently, other investigators have also shown that P. gingivalis induces NF κ B activation and p38 signaling for its actions [61, 62]. An inhibitor against MEK1/2 signaling pathway suppressed completely the IL-1 β -induced stimulation of NAMPT expression.…”

Section: Discussionmentioning

confidence: 92%

“…P. gingivalis can invade host cells and also evade the host defense system [65–67]. As it has been shown in several cells that COX2, an enzyme which is responsible for the formation of prostanoids, is upregulated by P. gingivalis and IL-1 β , we also analyzed the COX2 expression as a positive control in our study [61, 62, 68, 69]. As expected, P. gingivalis and IL-1 β increased the COX2 expression in a dose- and time-dependent manner in PDL cells.…”

Section: Discussionmentioning

confidence: 99%

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Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Nokhbehsaim

Eick

Nogueira

et al. 2013

Mediators of Inflammation

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Periodontitis is an inflammatory disease caused by pathogenic microorganisms and characterized by the destruction of the periodontium. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), may be a pathomechanistic link between both diseases. The aim of this in vitro study was to examine the regulation of periodontal ligament (PDL) cells by NAMPT and its production under inflammatory and infectious conditions. NAMPT caused a significant upregulation of 9 genes and downregulation of 3 genes, as analyzed by microarray analysis. Eight of these genes could be confirmed by real-time PCR: NAMPT induced a significant upregulation of EGR1, MMP-1, SYT7, ITPKA, CCL2, NTM, IGF2BP3, and NRP1. NAMPT also increased significantly the MMP-1 and CCL2 protein synthesis. NAMPT was significantly induced by interleukin-1β and the periodontal microorganism P. gingivalis. NAMPT may contribute to periodontitis through upregulation of MMP-1 and CCL2 in PDL cells. Increased NAMPT levels, as found in obesity, may therefore represent a mechanism whereby obesity could confer an increased risk of periodontitis. Furthermore, microbial and inflammatory signals may enhance the NAMPT synthesis in PDL cells and thereby contribute to the increased gingival and serum levels of this adipokine, as found in periodontitis.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Nokhbehsaim

Eick

Nogueira

et al. 2013

Mediators of Inflammation

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“…These molecules play important roles in cell differentiation, proliferation and death [15], and are activated by phosphorylation of tyrosine/threonine residues in signal transduction cascades. Previous studies have shown that the p38 MAPK and ERK1/2 pathways are involved in the proliferation and differentiation of osteoblasts [16–18]. Therefore, we hypothesized that ODN MT01 might regulate the differentiation of osteoblastic cells via the MAPKs pathway.…”

Section: Introductionmentioning

confidence: 93%

A Specific Oligodeoxynucleotide Promotes the Differentiation of Osteoblasts via ERK and p38 MAPK Pathways

Shen

Zhang

et al. 2012

IJMS

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A specific oligodeoxynucleotide (ODN), ODN MT01, was found to have positive effects on the proliferation and activation of the osteoblast-like cell line MG 63. In this study, the detailed signaling pathways in which ODN MT01 promoted the differentiation of osteoblasts were systematically examined. ODN MT01 enhanced the expression of osteogenic marker genes, such as osteocalcin and type I collagen. Furthermore, ODN MT01 activated Runx2 phosphorylation via ERK1/2 mitogen-activated protein kinase (MAPK) and p38 MAPK. Consistently, ODN MT01 induced up-regulation of osteocalcin, alkaline phosphatase (ALP) and type I collagen, which was inhibited by pre-treatment with the ERK1/2 inhibitor U0126 and the p38 inhibitor SB203580. These results suggest that the ERK1/2 and p38 MAPK pathways, as well as Runx2 activation, are involved in ODN MT01-induced up-regulation of osteocalcin, type I collagen and the activity of ALP in MG 63 cells.

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“…Experimental animals models of oral infection cannot efficiently represent human oral pathogenic bacteria, 15,16 whereas human experimental studies may answer questions regarding the initiation of these diseases, 17 but difficult to identify mechanisms that convert protective inflammation to tissue destructive lesion, due to ethical considerations. Most studies using in vitro models have only employed single oral bacterial species to challenge 2-dimensional monolayer cells, 18,19 or cells in suspension, [20][21][22] despite that periodontal infections are biofilm-related. 23 Moreover, monolayer cell culture systems do not adequately mimic the morphological and functional features of primary gingival tissues.…”

Section: Introductionmentioning

confidence: 99%

Establishment of an oral infection model resembling the periodontal pocket in a perfusion bioreactor system

et al. 2015

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Periodontal infection involves a complex interplay between oral biofilms, gingival tissues and cells of the immune system in a dynamic microenvironment. A humanized in vitro model that reduces the need for experimental animal models, while recapitulating key biological events in a periodontal pocket, would constitute a technical advancement in the study of periodontal disease. The aim of this study was to use a dynamic perfusion bioreactor in order to develop a gingival epithelial-fibroblast-monocyte organotypic co-culture on collagen sponges. An 11 species subgingival biofilm was used to challenge the generated tissue in the bioreactor for a period of 24 h. The histological and scanning electron microscopy analysis displayed an epithelial-like layer on the surface of the collagen sponge, supported by the underlying ingrowth of gingival fibroblasts, while monocytic cells were also found within the sponge mass. Bacterial quantification of the biofilm showed that in the presence of the organotypic tissue, the growth of selected biofilm species, especially Campylobacter rectus, Actinomyces oris, Streptococcus anginosus, Veillonella dispar, and Porphyromonas gingivalis, was suppressed, indicating a potential antimicrobial effect by the tissue. Multiplex immunoassay analysis of cytokine secretion showed that interleukin (IL)-1 β, IL-2, IL-4, and tumor necrosis factor (TNF)-α levels in cell culture supernatants were significantly up-regulated in presence of the biofilm, indicating a positive inflammatory response of the organotypic tissue to the biofilm challenge. In conclusion, this novel host-biofilm interaction organotypic model might resemble the periodontal pocket and have an important impact on the study of periodontal infections, by minimizing the need for the use of experimental animal models.

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Porphyromonas gingivalis induces RANKL in bone marrow stromal cells: Involvement of the p38 MAPK

Cited by 13 publications

References 35 publications

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

A Specific Oligodeoxynucleotide Promotes the Differentiation of Osteoblasts via ERK and p38 MAPK Pathways

Establishment of an oral infection model resembling the periodontal pocket in a perfusion bioreactor system

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