Porphyromonas gingivalis-induced inflammatory mediator profile in anex vivohuman whole blood model

Bodet, Charles; Chandad, Fatiha; Grenier, Daniel

doi:10.1111/j.1365-2249.2005.02956.x

Cited by 44 publications

(41 citation statements)

References 52 publications

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“…A previous report showed that MCP-1 expression was upregulated in P. gingivalis infected human umbilical vein endothelial cells [40]. Another study showed that P. gingivalis induced MCP-1 in an ex vivo human whole-blood model [41]. In the present study, our immunohistochemical results showed that the expression of MCP-1 in the neointimal area was enhanced in the P. gingivalis infected group compared to the non-infected group.…”

Section: Discussionsupporting

confidence: 69%

Porphyromonas gingivalis Accelerates Neointimal Formation after Arterial Injury

Kobayashi¹,

Suzuki²,

Ogawa³

et al. 2012

J Vasc Res

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Background: Inflammation plays a key role in neointimal hyperplasia after an arterial injury. Chronic infectious disorders, such as periodontitis, are associated with an increased risk of cardiovascular diseases. However, the effects of a periodontal infection on vascular remodeling have not been examined. We assess the hypothesis that periodontal infection could promote neointimal formation after an arterial injury. Methods: Mice were implanted with subcutaneous chambers (n = 41). Two weeks after implantation, the femoral arteries were injured, and Porphyromonas gingivalis (n = 21) or phosphate-buffered saline (n = 20) was injected into the chamber. The murine femoral arteries were obtained for the histopathological analysis. The expression level of mRNA in the femoral arteries was analyzed using quantitative reverse transcriptase polymerase chain reaction (n = 19–20). Results: The intima/media thickness ratio in the P. gingivalis infected group was found to be significantly increased in comparison to the non-infected group. The expression of matrix metalloproteinase-2 mRNA was significantly increased in the P. gingivalis infected group compared to the non-infected group. Conclusion: These findings demonstrate that P. gingivalis injection can promote neointimal formation after an arterial injury. Periodontitis may be a critical factor in the development of restenosis after arterial intervention.

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Section: Discussionsupporting

confidence: 69%

Porphyromonas gingivalis Accelerates Neointimal Formation after Arterial Injury

Kobayashi¹,

Suzuki²,

Ogawa³

et al. 2012

J Vasc Res

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“…Among other cells, Jurkat T-cells are also known to produce PGE 2 [33][34][35]. It has been shown that P. gingivalis can induce PGE 2 production in a variety of cell types, including gingival fibroblasts [36], epithelial cells and macrophages [37], osteoblasts [20], bone marrow stromal cells [19], as well as whole blood cells [38]. The present study demonstrates that P. gingivalis enhances PGE 2 production in Jurkat T-cells as well, concomitantly to RANKL.…”

Section: Discussionsupporting

confidence: 61%

Porphyromonas gingivalis Induces RANKL in T-cells

2010

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Porphyromonas gingivalis is an oral pathogen highly implicated in chronic periodontitis, a disease characterized by inflammatory destruction of the tooth-supporting alveolar bone and eventually, tooth loss. T-cell innate immune responses are actively involved in this pathological process. Receptor activator of NF-kappaB Ligand (RANKL) is a cytokine that stimulates bone resorption, while its soluble decoy receptor osteoprotegerin (OPG) blocks its action. This study aimed to investigate in Jurkat T-cells the effects of P. gingivalis on the RANKL-OPG system and the major inflammatory mediator of bone resorption prostaglandin E(2) (PGE(2)). P. gingivalis caused concentration-dependent up-regulation of RANKL gene expression and protein production, assessed by quantitative PCR and ELISA, respectively. PGE(2) production was also enhanced. However, OPG was not detected. In conclusion, P. gingivalis induces RANKL and PGE(2) in T-cells, potentially favoring bone resorption. These T-cell responses to P. gingivalis may contribute to the pathogenesis of inflammatory alveolar bone destruction occurring in chronic periodontitis. ABSTRACTPorphyromonas gingivalis is an oral pathogen highly implicated in chronic periodontitis, a disease characterised by inflammatory destruction of the toothsupporting alveolar bone, and eventually tooth loss. T-cell innate immune responses are actively involved in this pathological process. Receptor Activator of NF-κB Ligand (RANKL) is a cytokine that stimulates bone resorption, while its soluble decoy receptor osteoprotegerin (OPG) blocks its action. This study aimed to investigate in Jurkat T-cells the effects of P. gingivalis on the RANKL-OPG system and the major inflammatory mediator of bone resorption prostaglandin E 2 (PGE 2 ). P. gingivalis caused concentration-dependent up-regulation of RANKL gene expression and protein production, assessed by quantitative PCR and ELISA, respectively. PGE 2 production was also enhanced. However, OPG was not detected. In conclusion, P. gingivalis induces RANKL and PGE 2 in T-cells, potentially favouring bone resorption. These T-cell responses to P. gingivalis may contribute to the pathogenesis of inflammatory alveolar bone destruction occurring in chronic periodontitis.

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“…RANTES was detected at significantly higher levels in gingival crevicular fluid from chronic periodontitis and generalized aggressive periodontitis, and it was positively correlated with both probing depth and clinical attachment loss (44,45). P. gingivalis induced the secretion of RANTES from human whole blood (46). Periodontitis is among the most prevalent chronic diseases in humans, and up-regulation of IP-10 and RANTES by bacterial components may contribute to the progression of this disease.…”

Section: Discussionmentioning

confidence: 99%

The Major Outer Membrane Protein of a Periodontopathogen Induces IFN-β and IFN-Stimulated Genes in Monocytes via Lipid Raft and TANK-Binding Kinase 1/IFN Regulatory Factor-3

Lee

Kim²,

Jun³

et al. 2009

The Journal of Immunology

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Surface molecules of pathogens play an important role in stimulating host immune responses. Elucidation of the signaling pathways activated by critical surface molecules in host cells provides insight into the molecular pathogenesis resulting from bacteria-host interactions. MspTL is the most abundant outer membrane protein of Treponema lecithinolyticum, which is associated with periodontitis, and induces expression of a variety of proinflammatory factors. Although bacteria and bacterial components like LPS and flagellin are known to induce IFN-β, induction by bacterial surface proteins has not been reported. In the present study, we investigated MspTL-mediated activation of signaling pathways stimulating up-regulation of IFN-β and IFN-stimulated genes in a human monocytic cell line, THP-1 cells, and primary cultured human gingival fibroblasts. MspTL treatment of the cells induced IFN-β and the IFN-stimulated genes IFN-γ-inducible protein-10 (IP-10) and RANTES. A neutralizing anti-IFN-β Ab significantly reduced the expression of IP-10 and RANTES, as well as STAT-1 activation, which was also induced by MspTL. Experiments using specific small interfering RNA showed that MspTL activated TANK-binding kinase 1 (TBK1), but not inducible IκB kinase (IKKi). MspTL also induced dimerization of IFN regulatory factor-3 (IRF-3) and translocation into the nucleus. The lipid rapid-disrupting agents methyl-β-cyclodextrin, nystatin, and filipin inhibited the MspTL internalization and cellular responses, demonstrating that lipid raft activation was a prerequisite for MspTL cellular signaling. Our results demonstrate that MspTL, the major outer protein of T. lecithinolyticum, induced IFN-β expression and subsequent up-regulation of IP-10 and RANTES via TBK1/IRF-3/STAT-1 signaling secondary to lipid raft activation.

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Porphyromonas gingivalis-induced inflammatory mediator profile in anex vivohuman whole blood model

Cited by 44 publications

References 52 publications

<b><i>Porphyromonas gingivalis</i></b> Accelerates Neointimal Formation after Arterial Injury

<b><i>Porphyromonas gingivalis</i></b> Accelerates Neointimal Formation after Arterial Injury

Porphyromonas gingivalis Induces RANKL in T-cells

The Major Outer Membrane Protein of a Periodontopathogen Induces IFN-β and IFN-Stimulated Genes in Monocytes via Lipid Raft and TANK-Binding Kinase 1/IFN Regulatory Factor-3

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