<i>Porphyromonas gingivalis</i>stimulates monocyte adhesion to human umbilical vein endothelial cells

Hashizume, Tomomi; Kurita‐Ochiai, Tomoko; Yamamoto, Masafumi

doi:10.1111/j.1574-695x.2011.00786.x

Cited by 28 publications

(33 citation statements)

References 33 publications

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“…In preparation for this study, we ran experiments with MOIs of 10, 100, and 1,000 (data not shown). Results of studies using various MOIs, including the MOIs of 10 (18), 100 (19,20), and 1,000 (18), have been previously reported in the literature. The optimum concentration achieved in our experiments-in line with most publications in the literature-was the MOI of 100.…”

Section: Methodsmentioning

confidence: 99%

Endothelial Cell Response to Fusobacterium nucleatum

Mendes

Nguyen²,

Stephens³

et al. 2016

Infect Immun

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c Vascular response is an essential aspect of an effective immune response to periodontal disease pathogens, as new blood vessel formation contributes to wound healing and inflammation. Gaining a greater understanding of the factors that affect vascular response may then contribute to future breakthroughs in dental medicine. In this study, we have characterized the endothelial cell response to the common bacterium Fusobacterium nucleatum, an important bridging species that facilitates the activity of late colonizers of the dental biofilm. Endothelial cells were infected with Fusobacterium nucleatum (strain 25586) for periods of 4, 12, 24, or 48 h. Cell proliferation and tube formation were analyzed, and expression of adhesion molecules (CD31 and CD34) and vascular endothelial growth factor (VEGF) receptors 1 and 2 was measured by fluorescenceactivated cell sorter (FACS) analysis. Data indicate that F. nucleatum impaired endothelial cell proliferation and tube formation. The findings suggest that the modified endothelial cell response acts as a mechanism promoting the pathogenic progression of periodontal diseases and may potentially suggest the involvement of periodontopathogens in systemic diseases associated with periodontal inflammation.

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Section: Methodsmentioning

confidence: 99%

Endothelial Cell Response to Fusobacterium nucleatum

Mendes

Nguyen²,

Stephens³

et al. 2016

Infect Immun

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“…Increased expression of Eselectin and production of proinflammatory cytokines in the endothelium play a pivotal role in the generation of leukocyte infiltrates and subsequent atherosclerotic plaque formation (16,28). P. gingivalis infection significantly increases endothelial expression of VCAM-1, ICAM-1, and E-selectin, enhances production of interleukin-6 (IL-6), IL-8, and monocyte chemoattractant protein 1 (MCP-1), and increases adhesion of THP-1 monocytes to endothelial cells (18,46). Therefore, P. gingivalis elicits a proatherogenic response in endothelial cells.…”

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confidence: 99%

E-Selectin Mediates Porphyromonas gingivalis Adherence to Human Endothelial Cells

et al. 2012

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ABSTRACTPorphyromonas gingivalis, a major periodontal pathogen, may contribute to atherogenesis and other inflammatory cardiovascular diseases. However, little is known about interactions betweenP. gingivalisand endothelial cells. E-selectin is a membrane protein on endothelial cells that initiates recruitment of leukocytes to inflamed tissue, and it may also play a role in pathogen attachment. In the present study, we examined the role of E-selectin inP. gingivalisadherence to endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with tumor necrosis factor alpha (TNF-α) to induce E-selectin expression. Adherence ofP. gingivalisto HUVECs was measured by fluorescence microscopy. TNF-α increased adherence of wild-typeP. gingivalisto HUVECs. Antibodies to E-selectin and sialyl Lewis X suppressedP. gingivalisadherence to stimulated HUVECs.P. gingivalismutants lacking OmpA-like proteins Pgm6 and -7 had reduced adherence to stimulated HUVECs, but fimbria-deficient mutants were not affected. E-selectin-mediatedP. gingivalisadherence activated endothelial exocytosis. These results suggest that the interaction between host E-selectin and pathogen Pgm6/7 mediatesP. gingivalisadherence to endothelial cells and may trigger vascular inflammation.

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“…The results demonstrated that biochanin A inhibited the expression of TNF-α and IL-8 in LPS-stimulated human vascular endothelial cells in a dose-dependent manner. The adhesion of neutrophils to the endothelium is a crucial step in the inflammatory response which precedes the development of atherosclerosis [12]. VCAM-1, ICAM-1 and E-selectin recruit leukocytes to the sites of inflammation [36].…”

Section: Discussionmentioning

confidence: 99%