The effect of <i>Porphyromonas gingivalis</i> infection on cytokine levels in type 2 diabetic mice

Nishihara, R.; Sugano, Naoyuki; Takano, M.; Shimada, Tadashi; Tanaka, Hideki; Oka, Shogo; Ito, Koichi

doi:10.1111/j.1600-0765.2008.01130.x

Cited by 34 publications

(33 citation statements)

References 36 publications

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“…The alteration in serum levels of adiponectin according to periodontal status and the effect of adiponectin on periodontopathogen-induced cytokine expression by macrophages and osteoclast formation have been estimated [23-25], but few studies have addressed the effect of adiponectin on the cells of periodontal tissue such as PDL and gingival fibroblasts. In this study, it was shown that PDL and gingival fibroblasts express AdipoR1 and that gAd does not affect the production of IL-6 and IL-8 in those cells.…”

Section: Discussionmentioning

confidence: 99%

“…One study found a trend toward decreased serum levels of adiponectin in periodontitis patients [22]. Moreover, infection with periodontopathogen such as Porphyromonas gingivalis was shown to cause decreased serum levels of adiponectin in type 2 diabetic mice [23]. In another study, antimicrobial periodontal treatment (APT) not only ameliorated periodontitis but also increased serum levels of adiponectin in type 2 diabetes mellitus patients.…”

Section: Introductionmentioning

confidence: 99%

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Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts

Park

Bak

Kim

et al. 2011

J Periodontal Implant Sci

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PurposeGlobular adiponectin (gAd) is a type of adipocytokine, which is mainly produced by adipose tissue. It has been reported that gAd acts as a pro- as well as an anti-inflammatory factor. Interleukin (IL)-6 and IL-8 are pro-inflammatory cytokines. To investigate the role of gAd on periodontal tissues, the expression of adiponectin receptor 1 (AdipoR1) and the effect of gAd on the expression of IL-6 and IL-8 were investigated in periodontal ligament (PDL) and gingival fibroblasts.MethodsPDL and gingival fibroblasts were cultured from human periodontal tissues. gAd derived from Escherichia coli and murine myeloma cells were used. The expression of AdipoR1 was estimated by reverse transcription-polymerase chain reaction and western blot. The expression of cytokines was measured by enzyme-linked immunosorbent assay.ResultsPDL and gingival fibroblasts expressed both mRNA and protein of AdipoR1. gAd derived from E. coli increased the production of IL-6 and IL-8, but polymyxin B, an inhibitor of lipopolysaccharide (LPS), inhibited IL-6 and IL-8 production induced by gAd in both types of cells. gAd derived from murine myeloma cells did not induce IL-6 and IL-8 production in those cells. gAd derived from E. coli contained higher levels of LPS than gAd derived from murine myeloma cells. LPS increased production of IL-6 and IL-8 in PDL and gingival fibroblasts, but pretreatment of cells with gAd derived from murine myeloma cells did not inhibit LPS-induced IL-6 and IL-8 expression.ConclusionsOur results suggest that PDL and gingival fibroblasts express AdipoR1 and that gAd does not act as a modulator of IL-6 and IL-8 expression in PDL and gingival fibroblasts.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts

Park

Bak

Kim

et al. 2011

J Periodontal Implant Sci

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“…The authors postulated that glycaemic control in patients with periodontitis and diabetes is potentially influenced by the persistence of P. gingivalis, particularly clones with type II fimbriae, following treatment (Makiura et al 2008). It has also been reported in in vitro studies that cytokine induction (specifically IL-1b, IL-8, IL-12 and TNF-a) by P. gingivalis with type II fimbriae is greater than that induced by P. gingivalis with type I fimbriae (Sugano et al 2004), and in animal studies that P. gingivalis inoculation can lead to elevated serum levels of TNF-a and IL-6 (Nishihara et al 2009). Clearly, more research is required, integrating both microbial assessment and analysis of serum cytokine levels.…”

Section: Microbial Factorsmentioning

confidence: 94%

“…A number of studies of animal models have highlighted the importance of TNF-a in possibly prolonging the immune response to plaque bacteria in both T1DM and T2DM and thereby promoting periodontitis in these conditions (Lalla et al 2000a,b, Graves et al 2004, Naguib et al 2004, Liu et al 2006a,b, Watanabe et al 2008, Pacios et al 2012. The role of TNF-a (and IL-6) in the enhanced immune responses to periodontal bacteria in diabetic mouse models has also been highlighted (Graves et al 2005, Nishihara et al 2009, Takano et al 2010). However, evidence for any association between levels of TNF-a in oral fluids or gingival tissues and T2DM in chronic periodontitis is inconsistent (Duarte et al 2007b, Navarro-Sanchez et al 2007, Ross et al 2010, Santos et al 2010b.…”

Section: Cytokines and Adipokinesmentioning

confidence: 99%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

217

258

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A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes.Abstract Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

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“…), and in animal studies that P. gingivalis inoculation can lead to elevated serum levels of TNF‐α and IL‐6 (Nishihara et al. ). Clearly, more research is required, integrating both microbial assessment and analysis of serum cytokine levels.…”

Section: The Impact Of Periodontal Disease On Diabetesmentioning

confidence: 99%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

J Clinic Periodontology

352

127

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Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

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The effect of Porphyromonas gingivalis infection on cytokine levels in type 2 diabetic mice

Abstract: These observations suggest that tumor necrosis factor-alpha, interleukin-6 and adiponectin are an integral part of the link between diabetes mellitus and Porphyromonas gingivalis infection.

Cited by 34 publications

References 36 publications

Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts

Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

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