<i>Porphyromonas gingivalis</i> Fimbriae Induce Adhesion of Monocytic Cell Line U937 to Endothelial Cells

Hirose, Koichi; Isogai, Emiko; Ueda, Itsuo

doi:10.1111/j.1348-0421.2000.tb01241.x

Cited by 15 publications

(8 citation statements)

References 24 publications

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“…We evaluated ICAM-1 expression by performing Western blot and qRT-PCR in endothelial cells infected with P. gingivalis for 24 h at an MOI of 100. Our prior work found that ICAM-1 expression and monocyte-endothelial cell adhesion were increased when endothelial cells were infected with P. gingivalis , which is consistent with the results of others [ 36 , 37 ]. In the presence of ISO-1, both the ICAM-1 protein and mRNA level induced by P. gingivalis infection were significantly decreased.…”

Section: Discussionsupporting

confidence: 92%

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Xu¹,

Pan²,

Xu³

et al. 2018

BMC Microbiol

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BackgroundPorphyromonas gingivalis (P. gingivalis), one of the main pathogenic bacteria involved in periodontitis, induces the expression of intercellular adhesion molecule − 1 (ICAM-1) and monocyte-endothelial cell adhesion. This effect plays a pivotal role in atherosclerosis development. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and critically affects atherosclerosis pathogenesis. In this study, we tested the involvement of MIF in the P. gingivalis ATCC 33277-enhanced adhesive properties of endothelial cells.ResultsEndothelial MIF expression was enhanced by P. gingivalis ATCC 33277 infection. The MIF inhibitor ISO-1 inhibited ICAM-1 production in endothelial cells, and monocyte-endothelial cell adhesion was induced by P. gingivalis ATCC 33277 infection. However, the addition of exogenous human recombinant MIF to P. gingivalis ATCC 33277-infected endothelial cells facilitated monocyte recruitment by promoting ICAM-1 expression in endothelial cells.ConclusionsThese experiments revealed that MIF in endothelial cells participates in the pro-atherosclerotic lesion formation caused by P. gingivalis ATCC 33277 infection. Our novel findings identify a more detailed pathological role of P. gingivalis ATCC 33277 in atherosclerosis.

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Section: Discussionsupporting

confidence: 92%

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Xu¹,

Pan²,

Xu³

et al. 2018

BMC Microbiol

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“…Furthermore, the ability of P. gingivalis to invade primary gingival epithelial cells has been correlated with fimA expression (43). P. gingivalis fimbriae have also been reported to induce the expression of inflammatory cytokines in human gingival fibroblasts and mouse peritoneal macrophages and to induce monocyte adhesion to HUVEC (18,19,(31)(32)(33)(34)(35). A recent study has demonstrated that P. gingivalis fimbriae use molecules of the ␤-2 integrin family (CD18) on mouse macrophages as cellular receptors and that CD18 may play a functional role in signaling for the fimbria-induced expression of IL-1␤ and tumor necrosis factor from these cells (40).…”

Section: Discussionmentioning

confidence: 99%

Fimbria-Dependent Activation of Cell Adhesion Molecule Expression in Porphyromonas gingivalis -Infected Endothelial Cells

et al. 2002

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Porphyromonas gingivalis is an oral pathogen that has recently been associated with chronic inflammatory diseases such as atherosclerosis. The strength of the epidemiological associations of P. gingivalis with atherosclerosis can be increased by the demonstration that P. gingivalis can initiate and sustain growth in human vascular cells. We previously established that P. gingivalis can invade aortic, heart, and human umbilical vein endothelial cells (HUVEC), that fimbriae are required for invasion of endothelial cells, and that fimbrillin peptides can induce the expression of the chemokines interleukin 8 and monocyte chemotactic protein. In this study, we examined the expression of surface-associated cell adhesion molecules on endothelial cells in response to P. gingivalis infection by fluorescence-activated cell sorting FACS analysis and confocal microscopy. Coculture of HUVEC with P. gingivalis strain 381 or A7436 resulted in the induction in the expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and P-and Eselectins, which was maximal at 48 h postinfection. In contrast, we did not observe induction of ICAM-1, VCAM-1, or P-or E-selectin expression in HUVEC cultured with the noninvasive P. gingivalis fimA mutant DPG3 or when P. gingivalis was incubated with fimbrillin peptide-specific anti-sera prior to the addition to HUVEC. Furthermore, the addition of a peptide corresponding to the N-terminal domain of fimbrillin to HUVEC resulted in an increase in ICAM-1, VCAM-1, and P-and E-selectins, which was maximal at 48 h and similar to that observed for live P. gingivalis. Treatment of P. gingivalis-infected HUVEC with cytochalsin D, which prevented P. gingivalis invasion, also resulted in the inhibition of ICAM-1, VCAM-1, or P-and E-selectin expression. Taken together, these results indicate that active P. gingivalis invasion of HUVEC mediated via the major fimbriae stimulates surface-associated cell adhesion molecule expression. Stimulation of adhesion molecules involved in the recruitment of leukocytes to sites of inflammation by P. gingivalis may play a role in the pathogenesis of systemic inflammatory diseases associated with this microorganism, including atherosclerosis.

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“…In addition, the presence of P. gingivalis fimbriae has been demonstrated to increase the attachment of macrophages to endothelial cells in vitro. 22 This could result from the increased expression of adhesion receptors such as ICAM-1 from the endothelial cells in the presence of bacteria. 14 One of the consequences of increased endothelial NADH oxidase activity induced in the presence of P. gingivalis could be an increase in oxLDL levels, which also have been demonstrated to increase the adhesiveness of endothelial cells.…”

Section: Oral Bacteria-induced Foam Cell Formationmentioning

confidence: 99%

Role for Periodontal Bacteria in Cardiovascular Diseases

et al. 2001

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Porphyromonas gingivalis Fimbriae Induce Adhesion of Monocytic Cell Line U937 to Endothelial Cells

Cited by 15 publications

References 24 publications

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Fimbria-Dependent Activation of Cell Adhesion Molecule Expression in Porphyromonas gingivalis -Infected Endothelial Cells

Role for Periodontal Bacteria in Cardiovascular Diseases

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