Cyclooxygenase‐2‐Dependent Prostaglandin Production by Peripheral Blood Monocytes Stimulated With Lipopolysaccharides Isolated From Periodontopathogenic Bacteria

Noguchi, Kazuyuki; Yanai, Masayuki; Shitashige, Miki; Nishihara, Tatsuji; Ishikawa, Isao

doi:10.1902/jop.2000.71.10.1575

Cited by 21 publications

(16 citation statements)

References 50 publications

(48 reference statements)

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“…In periodontitis, increased levels of gingival crevicular fluid (GCF) PGE 2 have been predictive of longitudinal periodontal attachment loss (Offenbacher et al ., 1986), and associated with the clinical signs of bleeding on probing (Zhong et al, 2007), both of which would suggest that increased PGE 2 expression is associated with progressive lesions (Champagne et al ., 2003). The biosynthesis of PGE 2 and other prostanoids is tightly coupled to the inducible expression of COX-2, and the transcriptional control of COX-2 levels appears to be the key regulatory gate for modulating tissue PGE 2 levels (Noguchi et al, 2000). Although levels of PGE 2 increase during certain stages of disease progression, little is known regarding the regulation of local PGE 2 synthesis, in which some down-regulation must be needed to prevent a continued and ever-expansive loss of connective tissue.…”

Section: Introductionmentioning

confidence: 99%

Alteration of PTGS2 Promoter Methylation in Chronic Periodontitis

et al. 2009

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Levels of prostaglandin E 2 and the prostaglandin-endoperoxide synthase-2 (PTGS2, or COX-2) increase in actively progressing periodontal lesions, but decrease in chronic disease. We hypothesized that chronic inflammation is associated with altered DNA methylation levels within the PTGS2 promoter, with effects on COX-2 mRNA expression. PTGS2 promoter methylation levels from periodontally inflamed gingival biopsies showed a 5.06-fold increase as compared with non-inflamed samples (p = 0.03), and the odds of methylation in a CpG site in the inflamed gingival group is 4.46 times higher than in the same site in the non-inflamed group (p = 0.016). The level of methylation at −458 bp was inversely associated with transcriptional levels of PTGS2 (RT-PCR) (p = 0.01). Analysis of the data suggests that, in chronically inflamed tissues, there is a hypermethylation pattern of the PTGS2 promoter in association with a lower level of PTGS2 transcription, consistent with a dampening of COX-2 expression in chronic periodontitis. These findings suggest that the chronic persistence of the biofilm and inflammation may be associated with epigenetic changes in local tissues at the biofilm-gingival interface.

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Section: Introductionmentioning

confidence: 99%

Alteration of PTGS2 Promoter Methylation in Chronic Periodontitis

et al. 2009

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“…Meloxicam is a non-steroidal anti-inflammatory drug, a derivative from oxicam, and may be used as a selective COX-2 inhibitor 1 . Because of its selective action 16 , meloxicam has some advantages over the conventional anti-inflammatory drugs that act similarly on the COX-1 and COX-2 isoenzymes, because it reduces the damage in the gastric mucosa and does not change the platelet aggregation process 1 . The aim of the present study was to evaluate the effect of meloxicam, an agent that selectively inhibits COX-2, on the progression of alveolar bone loss in an experimental model of periodontitis in rats using radiographic analysis.…”

Section: Introductionmentioning

confidence: 99%

Selective cyclooxygenase-2 inhibition prevents bone resorption

Nassar

Nassar³

et al. 2005

Braz. oral res.

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ABSTRACT:The aim of the present work was to evaluate the effect of a selective cyclooxygenase-2 (COX-2) inhibitor (meloxicam) on the alveolar bone loss progression in experimentally induced periodontitis. Forty (40) Wistar rats were separated into 8 experimental groups (n = 5). Cotton ligatures were placed at the gingival margin level of the lower right first molars of some rats. Four groups were treated for 5 or 15 days with an oral dose of 15 mg/kg of body weight/day of the selective COX-2 inhibitor. The other groups were used as positive control (sham) or negative control in each experimental period. Standardized digital radiographs were taken after sacrifice at 5 and 15 days to measure the amount of bone loss at the mesial root surface of the first molar tooth in each rat. The treatment with meloxicam did not induce weight alteration or other visible systemic manifestations. One way analysis of variance (ANOVA) indicated that groups treated with meloxicam, after 5 days, had significantly less alveolar bone loss (p < 0.05) when compared with control groups. On the other hand, no significant differences in bone loss were observed after 15 days of treatment with meloxicam. These data provide evidence that systemic therapy with meloxicam can modify the progression of experimentally induced periodontitis in rats during the initial experimental period. DESCRIPTORS: Alveolar bone loss; Anti-inflammatory agents, non-steroidal; Cyclooxygenase inhibitors; Periodontitis; Radiography, dental. RESUMO:O objetivo deste trabalho foi avaliar o efeito de um inibidor seletivo da cicloxigenase-2 (COX-2) (meloxicam) na progressão da perda óssea alveolar durante o desenvolvimento da doença periodontal experimental induzida. Quarenta (40) ratos Wistar foram separados em 8 grupos experimentais (n = 5). Ligaduras de fio de algodão foram colocadas na margem gengival do primeiro molar inferior direito de alguns ratos. Quatro grupos foram tratados por 5 ou 15 dias com uma dose oral de 15 mg/kg de peso corporal/dia do inibidor seletivo de COX-2. Os outros grupos foram usados como controle positivo (sham) e controle negativo dentro de cada período experimental. Radiografias digitais padronizadas foram realizadas para medir a perda óssea na região mesial do primeiro molar inferior de cada rato. O efeito do tratamento com meloxicam não induziu alteração de peso ou outras manifestações sistêmicas visíveis. A Análise de Variância (ANOVA) indicou que os grupos tratados com meloxicam após 5 dias apresentaram perda óssea alveolar significativamente menor (p < 0,05). Por outro lado, a perda óssea não foi significativa após 15 dias de tratamento com meloxicam. Os dados apresentados no presente trabalho sugerem que o tratamento sistêmico com meloxicam pode modificar a progressão da periodontite experimental em ratos no período experimental inicial.

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“…The major signaling pathway of the EP3 receptor is inhibition of adenylate cyclase via Gi, but plural EP3 splicing variants exhibit various signaling pathways (Namba et al,1993). PGE 2 is produced by stromal cells and infiltrating mononuclear cells (Noguchi et al, 2000;Harizi et al, 2002). In an inflammatory environment, PGE 2 induces vasodilation and promotes tissue edema in cooperation with other mediators.…”

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confidence: 99%

E-Prostanoid (EP)2/EP4 Receptor-Dependent Maturation of Human Monocyte-Derived Dendritic Cells and Induction of Helper T2 Polarization

Kubo¹,

Takahashi²,

Takei³

et al. 2004

J Pharmacol Exp Ther

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Prostaglandin (PG) E 2 induces dendritic cell maturation in cooperation with proinflammatory cytokines [such as tumor necrosis factor (TNF)-␣ and interleukin (IL)-1␤]. To clarify the involvement of E-prostanoid (EP) receptors in the effect of prostaglandin E 2 on human monocyte-derived dendritic cell (MoDC) maturation, we examined the effect of four types of EP receptor-selective agonists on MoDC maturation. PGE 2 as well as 11,15-O-dimethyl prostaglandin (E 2 ONO-AE1-259-01) (EP2 receptor agonist) and ONO-AE1-329 (EP4 receptor agonist) concentration dependently enhanced the expression of CD80, CD86, CD83, and HLA-DR on MoDCs during maturation, especially in the presence of TNF-␣, whereas 17S-2,5-ethano-6-oxo-17,20-dimethyl prostaglandin E 1 (EP1 receptor agonist) and 16S-9-deoxy-9␤-chloro-15-deoxy-16-hyfroxy-17,17-trimethylene-19,20-didehydro prostaglandin F 2 (EP3 receptor agonist) showed no effect. The maximal effect of ONO-AE1-259-01 was higher than that of ONO-AE1-329; however, the stimulation with ONO-AE1-259-01 was less effective than that with PGE 2 . Simultaneous stimulation with both EP receptor agonists produced additive effects and 11-deoxy-PGE 1 (EP2/EP4 receptor mixed agonist) mimicked the effects of PGE 2 . Dibutyryl cAMP mimicked the effects of PGE 2 , indicating the mediation of PGE 2 action by cAMP. Matured MoDCs induced by PGE 2 or EP2 and/or EP4 receptor agonists showed a decrease in lipopolysaccharide (LPS)-stimulated IL-12p70, IL-6, and IL-10 production. The coculture of naive T cells with matured MoDCs induced under different conditions showed that EP2/EP4-stimulated MoDCs preferentially induced alloresponsive helper T (Th)2 cells. Together, it was concluded that the cooperative stimulation of EP2 and EP4 receptor subtypes by PGE 2 promoted MoDC maturation and inhibited LPS-induced cytokine production in MoDCs. The matured MoDCs under such conditions preferably induced Th2 polarization, indicating the importance of EP2 and EP4 receptors in the determination of Th1/Th2 development of naive T cells.

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Cyclooxygenase‐2‐Dependent Prostaglandin Production by Peripheral Blood Monocytes Stimulated With Lipopolysaccharides Isolated From Periodontopathogenic Bacteria

Cited by 21 publications

References 50 publications

Alteration of PTGS2 Promoter Methylation in Chronic Periodontitis

Alteration of PTGS2 Promoter Methylation in Chronic Periodontitis

Selective cyclooxygenase-2 inhibition prevents bone resorption

E-Prostanoid (EP)2/EP4 Receptor-Dependent Maturation of Human Monocyte-Derived Dendritic Cells and Induction of Helper T2 Polarization

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