Induction of monocyte chemoattractant protein-1 by Porphyromonas gingivalis in human endothelial cells

Kang, I

doi:10.1016/s0928-8244(02)00407-8

Cited by 21 publications

(32 citation statements)

References 28 publications

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“…Since the bacterial adhesion was not diminished by heat treatment, they suggested that P. gingivalis adhesion to epithelial cells was essential for cytokine responses. Other reports showed that infection with viable P. gingivalis induces MCP-1 expression in human epithelial cells (20,34). In these studies, heat-inactivated bacteria did not induce MCP-1 response, suggesting that invasion of viable P. gingivalis is necessary for chemokine production by epithelial cells.…”

Section: Discussionmentioning

confidence: 54%

“…Recent studies have found that infection with P. gingivalis induces IL-8 and MCP-1 responses in human endothelial cells at the mRNA level (4,20,34). At the same time, these reports also suggested that a high level of P. gingivalis To determine the numbers of adherent and invaded bacteria, the cultures were incubated for 1 h. Unattached bacteria were washed off with PBS, and the osteoblasts were disrupted by extensive pipetting with sterile water and then plated on blood agar plates.…”

Section: Vol 72 2004 P Gingivalis Induces Rankl Expression In Ostementioning

confidence: 99%

“…Previous studies suggested that adhesion and invasion of infected bacteria induce cellular responses (14,20,39,43,45,52). Activation of mitogen-activated protein kinase (MAPK) pathways has also shown to be involved in these proinflammatory responses; however, the mechanisms have not been elucidated (12,14,39,45,52).…”

mentioning

confidence: 99%

“…Activation of mitogen-activated protein kinase (MAPK) pathways has also shown to be involved in these proinflammatory responses; however, the mechanisms have not been elucidated (12,14,39,45,52). P. gingivalis can adhere to and invade epithelial and endothelial cells (3,5,6,9,10,26,33,35,44,56), and infection with viable organisms of P. gingivalis induces IL-1, IL-6, IL-8, TNF-␣, and monocyte chemoattractant protein 1 (MCP-1) production by human epithelial and endothelial cells (20,35,43). We found here that infection with viable P. gingivalis induced RANKL expression in osteoblasts through activator protein 1 (AP-1) signaling.…”

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confidence: 99%

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Porphyromonas gingivalisInduces Receptor Activator of NF-κB Ligand Expression in Osteoblasts through the Activator Protein 1 Pathway

Okahashi¹,

Inaba²,

Nakagawa³

et al. 2004

Infect Immun

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Porphyromonas gingivalis, an important periodontal pathogen, is closely associated with inflammatory alveolar bone resorption, and several components of the organism such as lipopolysaccharides have been reported to stimulate production of cytokines that promote inflammatory bone destruction. We investigated the effect of infection with viable P. gingivalis on cytokine production by osteoblasts. Reverse transcription-PCR and real-time PCR analyses revealed that infection with P. gingivalis induced receptor activator of nuclear factor B (NF-B) ligand (RANKL) mRNA expression in mouse primary osteoblasts. Production of interleukin-6 was also stimulated; however, osteoprotegerin was not. SB20350 (an inhibitor of p38 mitogen-activated protein kinase), PD98059 (an inhibitor of classic mitogen-activated protein kinase kinase, MEK1/2), wortmannin (an inhibitor of phosphatidylinositol 3 kinase), and carbobenzoxyl-leucinyl-leucinyl-leucinal (an inhibitor of NF-B) did not prevent the RANKL expression induced by P. gingivalis. Degradation of inhibitor of NF-B-alpha was not detectable; however, curcumin, an inhibitor of activator protein 1 (AP-1), prevented the RANKL production induced by P. gingivalis infection. Western blot analysis revealed that phosphorylation of c-Jun, a component of AP-1, occurred in the infected cells, and an analysis of c-Fos binding to an oligonucleotide containing an AP-1 consensus site also demonstrated AP-1 activation in infected osteoblasts. Infection with P. gingivalis KDP136, an isogenic deficient mutant of arginine-and lysine-specific cysteine proteinases, did not stimulate RANKL production. These results suggest that P. gingivalis infection induces RANKL expression in osteoblasts through AP-1 signaling pathways and cysteine proteases of the organism are involved in RANKL production.

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Section: Discussionmentioning

confidence: 54%

Section: Vol 72 2004 P Gingivalis Induces Rankl Expression In Ostementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Porphyromonas gingivalisInduces Receptor Activator of NF-κB Ligand Expression in Osteoblasts through the Activator Protein 1 Pathway

Okahashi¹,

Inaba²,

Nakagawa³

et al. 2004

Infect Immun

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“…A recent study reported similarities in the spectrum of bacteria in the oral cavity and in coronary plaques, and both diseases are characterized by an imbalanced immune reaction and a chronic inflammatory process [13], while significant similarities also exist in the pathogenetic processes of CVD and periodontitis, including monocyte hyperresponsiveness [38], elevations in systemic levels of C-reactive protein [34], serum amyloid A (SAA) [39], and fibrinogen [40].…”

Section: Introductionmentioning

confidence: 99%

Clinically Classified Periodontitis and Its Association in Patients with Preexisting Coronary Heart Disease

Chrysanthakopoulos

2013

Journal of Oral Diseases

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The aim of this retrospective study was to investigate possible associations between clinically classified periodontitis as determined by assessing its severity and diagnosed coronary heart disease in outpatients referred to a specialist clinic for neurosurgery treatment. A total of 2,912 individuals were clinically examined for periodontal disease experience by using probing pocket depth (PPD) and clinical attachment loss (CAL). Socioeconomic, oral health behaviour, and general health related information was collected by using a self-administered questionnaire. Statistical analysis of the questionnaire items was performed by using multivariate logistic regression analysis model. The results showed that the occurrence of hypertension (OR = 2.42, 95% CI = 1.52-3.84), smoking (OR = 1.97, 95% CI = 1.25-3.11), classified periodontitis (OR = 1.79, 95% CI = 1.15-2.77), and the high level of serum C-reactive protein (OR = 1.74, 95% CI = 1.05-2.89) were significantly associated with the presence of coronary heart disease. These observations strengthen the role of some of the traditional causative risk factors for coronary heart disease while a significant association was recorded between diagnosed coronary heart disease and clinically classified periodontitis which is considered as a risk factor for coronary heart disease.

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Effects of methyl gallate and gallic acid on the production of inflammatory mediators interleukin-6 and interleukin-8 by oral epithelial cells stimulated with Fusobacterium nucleatum

Kang

Jang

et al. 2009

J Microbiol.

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Interactions between periodontal bacteria and human oral epithelial cells can lead to the activation and expression of a variety of inflammatory mediators in epithelial cells. Fusobacterium nucleatum is a filamentous human pathogen that is strongly associated with periodontal diseases. This study examined the effects of methyl gallate (MG) and gallic acid (GA) on the production of inflammatory mediators, interleukin (IL)-6 and IL-8, by oral epithelial cells stimulated by F. nucleatum. In a real-time reverse transcription-polymerase chain reaction and an enzyme-linked immunosorbent assay, live F. nucleatum induced high levels of gene expression and protein release of IL-6 and IL-8. The effects of MG and GA were examined by treating KB oral epithelial cells with MG and GA and stimulating them with F. nucleatum. MG and GA inhibited significantly the increases in the IL-6 and IL-8 gene and protein levels in a dose-dependent manner. These Compounds also inhibited the growth of F. nucleatum. No visible effects of MG and GA on the adhesion and invasion of KB cells by F. nucleatum were observed. In conclusion, both MG and GA inhibit IL-6 and IL-8 production from F. nucleatum-activated KB cells.

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Induction of monocyte chemoattractant protein-1 by Porphyromonas gingivalis in human endothelial cells

Cited by 21 publications

References 28 publications

Porphyromonas gingivalisInduces Receptor Activator of NF-κB Ligand Expression in Osteoblasts through the Activator Protein 1 Pathway

Porphyromonas gingivalisInduces Receptor Activator of NF-κB Ligand Expression in Osteoblasts through the Activator Protein 1 Pathway

Clinically Classified Periodontitis and Its Association in Patients with Preexisting Coronary Heart Disease

Effects of methyl gallate and gallic acid on the production of inflammatory mediators interleukin-6 and interleukin-8 by oral epithelial cells stimulated with Fusobacterium nucleatum

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