Bioactive mechanism of Porphyromonas gingivalis lipid A

Ogawa, Tomohiko; Yagi, Takakazu

doi:10.1111/j.1600-0757.2009.00343.x

Cited by 20 publications

(22 citation statements)

References 59 publications

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“…It constitues an important component of the bacterial outer membrane ( Hamada et al, 1994 ). In general, the bacterial LPS consists of a distal polysaccharide (or O-antigen), a non-repeating “core” oligosaccharide and a hydrophobic domain known as lipid A (or endotoxin) ( Ogawa and Yagi, 2010 ; Figure 4 ). Lipid A, the inner-most component, is the biological active region of LPS that could cause deregulation of the mammalian innate immune system by interacting with both toll-like receptors 2 and 4 ( Darveau et al, 2004 ).…”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

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Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

2016

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Periodontal disease represents a group of oral inflammatory infections initiated by oral pathogens which exist as a complex biofilms on the tooth surface and cause destruction to tooth supporting tissues. The severity of this disease ranges from mild and reversible inflammation of the gingiva (gingivitis) to chronic destruction of connective tissues, the formation of periodontal pocket and ultimately result in loss of teeth. While human subgingival plaque harbors more than 500 bacterial species, considerable research has shown that Porphyromonas gingivalis, a Gram-negative anaerobic bacterium, is the major etiologic agent which contributes to chronic periodontitis. This black-pigmented bacterium produces a myriad of virulence factors that cause destruction to periodontal tissues either directly or indirectly by modulating the host inflammatory response. Here, this review provides an overview of P. gingivalis and how its virulence factors contribute to the pathogenesis with other microbiome consortium in oral cavity.

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Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

“… Schematic structure of lipopolysaccharide (LPS) of the outer membrane of P. gingivalis . Adapted from Ogawa and Yagi (2010) . …”

Section: Lipopolysaccharide (Lps)mentioning

confidence: 99%

Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

2016

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“…Recent studies have also shown that the purified or synthesized molecule of the lipid A is an agonist for TLR4/MD2, but it is relatively weak as an immunostimulant (32). It is now apparent that naturally derived P. gingivalis LPS as used in this study is recognized by both TLR2 and TLR4/MD2 (33). By blocking the TLR2 recognition of LP, the overall harmful effect of P. gingivalis could be prevented.…”

Section: Discussionmentioning

confidence: 99%

Blockade of TLR2 Inhibits Porphyromonas gingivalis Suppression of Mineralized Matrix Formation by Human Dental Pulp Stem Cells

Yamagishi

Torneck

Friedman

et al. 2011

Journal of Endodontics

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Introduction Human dental pulp stem/progenitor cells (hDPSC) can differentiate into odontoblast-like cells and express dentin sialophosphoprotein (DSPP) and osteocalcin (OCN); thus, they may be used to regenerate dentin. However, residual bacterial components in the root canal may suppress this activity. Purpose This study investigated the effect of a Porphyromonas gingivalis component on the expression of DSPP and OCN by stimulated hDPSCs and the influence of blockade of TLR2-mediated P. gingivalis host recognition. Methods Stimulated hDPSCs were exposed to varying concentrations of P. gingivalis lipopolysaccharide (LPS), and the expression of DSPP and OCN was measured. Similar groups of stimulated hDPSCs were exposed to TLR2 blocking agents before exposure to LPS. Results hDPSCs exposed to 5, 10, and 20 µg/mL LPS exhibited a dose-dependent reduction in the expression of DSPP (3.19 ± 0.18, 2.60 ± 0.49, and 1.15 ± 0.29, respectively) and OCN (3.51 ± 1.18, 2.60 ± 0.67 and 1.66 ± 0.89, respectively). The expression of DSPP and OCN after exposure to 20 µg/mL of LPS was significantly lower than measured for unexposed stimulated cells (analysis of variance and post hoc Tukey test, P < .05). The blockade of TLR2 using an extra- and intracellular agent affected DSPP (4.67 ± 0.97 and 5.29 ± 1.66, respectively) and OCN (5.25 ± 1.69 and 5.82 ± 2.38, respectively) expression at levels comparable to stimulated cells unexposed to 20 µg/mL LPS (6.32 ± 2.47 and 4.70 ± 1.60 for DSPP and OCN, respectively). Conclusions The suppressing effect of P. gingivalis on mineralized matrix formation by hDPSCs is confirmed, and this suppression can be moderated by TLR2 blockade.

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“…3-5). Previous studies have revealed discrepancies in the chemical structure of lipid A, the biologically active center of LPS, between P. gingivalis and E. coli LPS (32). In addition, it has previously been demonstrated that the endotoxic activities of P. gingivalis LPS and its lipid A are relatively weak when compared with those of E. coli-derived LPS and lipid A (4,13,32).…”

Section: Discussionmentioning

confidence: 99%

“…NF-κB has also been shown to be involved in the expression of adhesion molecules at the transcriptional level, in various cell types (19,20,30). Since it has been shown that discrepancies in chemical structures, immunobiological activities and the activation of intracellular signaling pathways exist between P. gingivalis and E. coli LPS (31,32), E. coli LPS was also introduced in the present study.…”

Section: Introductionmentioning

confidence: 99%

Role of JNK and NF-κB pathways in Porphyromonas gingivalis LPS-induced vascular cell adhesion molecule-1 expression in human aortic endothelial cells

Liu

Wang

Cheng

et al. 2013

Molecular Medicine Reports

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An increasing number of studies have shown a correlation between Porphyromonas gingivalis (P. gingivalis) infection and atherosclerosis. A recent study demonstrated that the expression of vascular cell adhesion molecule-1 (VCAM-1) was induced by P. gingivalis lipopolysaccharide (LPS) in human aortic endothelial cells (HAECs). The activation of p38 mitogen-activated protein kinase (p38 MAPK) was at least partially involved in this process. Those results suggested the potential involvement of P. gingivalis LPS in the pathogenesis of atherosclerosis. However, the mechanism involved in P. gingivalis LPS-induced VCAM-1 production has not yet been elucidated. The present study examined the role of the c-Jun N-terminal kinase (JNK) and nuclear factor‑κB (NF‑κB) cell signaling pathways in P. gingivalis LPS-induced VCAM-1 expression in HAECs. Western blotting was used to investigate the activation of JNK and NF‑κB pathways in HAECs exposed to P. gingivalis LPS. Following this, specific pharmacological inhibitors were introduced and the protein production of VCAM-1 was studied. The results showed that the JNK and NF‑κB pathways in HAECs were capable of being activated by P. gingivalis LPS. The inhibition of NF-κB by SN50 significantly attenuated P. gingivalis LPS-induced VCAM-1 expression, while the inhibition of JNK by SP600125 enhanced VCAM-1 expression in P. gingivalis LPS-treated HAECs. Therefore, the results indicated that NF‑κB was essential for the P. gingivalis LPS-induced VCAM-1 expression in HAECs and that JNK may be a suppressor of VCAM-1 expression in HAECs.

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Bioactive mechanism of Porphyromonas gingivalis lipid A

Cited by 20 publications

References 59 publications

Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line

Blockade of TLR2 Inhibits Porphyromonas gingivalis Suppression of Mineralized Matrix Formation by Human Dental Pulp Stem Cells

Role of JNK and NF-κB pathways in Porphyromonas gingivalis LPS-induced vascular cell adhesion molecule-1 expression in human aortic endothelial cells

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