Dense fimbrial meshwork enhances <i>Porphyromonas gingivalis</i> adhesiveness: a scanning electron microscopic study

Hongo, Hirohisa; Takano, Hiroko; Morita, Masato

doi:10.1111/j.1600-0765.2006.00922.x

Cited by 5 publications

(2 citation statements)

References 18 publications

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“…Fimbriae directly increase P. gingivalis adhesiveness by promoting inter-bacterial aggregation [34] [35] As CSE increases fimbrial density, we determined whether CSE promotes bacterial auto-aggregation. P. gingivalis , grown in GAM or CSE, was harvested by centrifugation and suspended in sterile PBS at O.D.…”

Section: Methodsmentioning

confidence: 99%

Tobacco Smoke Augments Porphyromonas gingivalis - Streptococcus gordonii Biofilm Formation

et al. 2011

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Smoking is responsible for the majority of periodontitis cases in the US and smokers are more susceptible than non-smokers to infection by the periodontal pathogen Porphyromonas gingivalis. P. gingivalis colonization of the oral cavity is dependent upon its interaction with other plaque bacteria, including Streptococcus gordonii. Microarray analysis suggested that exposure of P. gingivalis to cigarette smoke extract (CSE) increased the expression of the major fimbrial antigen (FimA), but not the minor fimbrial antigen (Mfa1). Therefore, we hypothesized that CSE promotes P. gingivalis-S. gordonii biofilm formation in a FimA-dependent manner. FimA total protein and cell surface expression were increased upon exposure to CSE whereas Mfa1 was unaffected. CSE exposure did not induce P. gingivalis auto-aggregation but did promote dual species biofilm formation, monitored by microcolony numbers and depth (both, p<0.05). Interestingly, P. gingivalis biofilms grown in the presence of CSE exhibited a lower pro-inflammatory capacity (TNF-α, IL-6) than control biofilms (both, p<0.01). CSE-exposed P. gingivalis bound more strongly to immobilized rGAPDH, the cognate FimA ligand on S. gordonii, than control biofilms (p<0.001) and did so in a dose-dependent manner. Nevertheless, a peptide representing the Mfa1 binding site on S. gordonii, SspB, completely inhibited dual species biofilm formation. Thus, CSE likely augments P. gingivalis biofilm formation by increasing FimA avidity which, in turn, supports initial interspecies interactions and promotes subsequent high affinity Mfa1-SspB interactions driving biofilm growth. CSE induction of P. gingivalis biofilms of limited pro-inflammatory potential may explain the increased persistence of this pathogen in smokers. These findings may also be relevant to other biofilm-induced infectious diseases and conditions.

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Section: Methodsmentioning

confidence: 99%

Tobacco Smoke Augments Porphyromonas gingivalis - Streptococcus gordonii Biofilm Formation

et al. 2011

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“…Electron microscopy studies have revealed that FimA constitutes a prominent surface molecule of P. gingivalis (11), perhaps being the first molecule of this pathogen coming into contact with epithelial cells. In this regard, oral gingival epithelial cells provide a physical barrier against invading bacteria and play an important role in the host's innate defense (1).…”

Section: Discussionmentioning

confidence: 99%

Differential Activation of Human Gingival Epithelial Cells and Monocytes by Porphyromonas gingivalis Fimbriae

2007

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Humans develop periodontitis in response to challenge by microbial dental plaque. Inflammation begins after perturbation of gingival epithelial cells by subgingival bacteria interacting through pattern-recognition receptors, including the Toll-like receptors (TLR). Porphyromonas gingivalis is a major periodontopathogen that interacts with epithelial cells through its cell surface fimbriae (FimA), leading to colonization and/or invasion. Previous work by our group has established membrane CD14 as an essential coreceptor for TLR2-mediated activation of transfected cell lines by P. gingivalis FimA. We have shown that gingival epithelial cells express TLR2 but not CD14 on their cell surfaces. We thus speculated that P. gingivalis FimA does not readily activate epithelial innate immune responses but rather functions to promote P. gingivalis colonization in the absence of a vigorous FimA-induced response. This hypothesis was verified by the findings that primary human gingival epithelial cells responded poorly to FimA in terms of interleukin (IL)-6, IL-8, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha responses, in stark contrast to the marked response to other TLR2 agonists (Pam3Cys, FSL-1) that are not strictly dependent on CD14. On the other hand, CD14-expressing human primary monocytes responded with high levels of the same cytokines to both FimA and the control TLR2 agonists. The gingival epithelial cells failed to respond to FimA even in the presence of exogenously added soluble CD14. These data indicate that the gingival epithelial cell hyporesponsiveness to FimA is attributable to the lack of membrane-expressed but not soluble CD14. In conclusion, P. gingivalis FimA differentially activates human monocytes and epithelial cells, perhaps reflecting different tactics used by P. gingivalis when interacting with different host cell types or a host strategy to limit inflammation.Porphyromonas gingivalis is a gram-negative, black-pigmented bacterium associated with periodontal disease, a condition which results in destruction of the tooth-supporting tissues and loss of teeth (16). P. gingivalis expresses virulence factors involved in host tissue destruction and immune perturbation (10). Adhesion molecules of P. gingivalis include fimbriae (FimA) and hemagglutinins; however, P. gingivalis FimA is considered a critical determinant for the attachment of this microorganism in the oral cavity (16). In this regard, there is strong evidence supporting a crucial role for FimA in P. gingivalis adhesion to several mammalian cells types; indeed, nonfimbriated mutants of P. gingivalis, constructed by inactivation of the FimA gene, display reduced adhesion and invasion of epithelial cells compared to wild-type P. gingivalis (29). Moreover, nonfimbriated mutants display a reduced ability to induce periodontal disease in mice following oral inoculation (19). In this context, P. gingivalis FimA has been shown to induce proinflammatory cytokine release in macrophages (22) as well as inflammatory bon...

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Peptide Mapping of a Functionally Versatile Fimbrial Adhesin from Porphyromonas gingivalis

Hajishengallis

2007

Int J Pept Res Ther

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Dense fimbrial meshwork enhances Porphyromonas gingivalis adhesiveness: a scanning electron microscopic study

Abstract: The results indicate that P. gingivalis adhesiveness is prominently enhanced by the dense fimbrial meshwork. Thus, the virulence of P. gingivalis is increased by the presence of rich fimbriae.

Cited by 5 publications

References 18 publications

Tobacco Smoke Augments Porphyromonas gingivalis - Streptococcus gordonii Biofilm Formation

Tobacco Smoke Augments Porphyromonas gingivalis - Streptococcus gordonii Biofilm Formation

Differential Activation of Human Gingival Epithelial Cells and Monocytes by Porphyromonas gingivalis Fimbriae

Peptide Mapping of a Functionally Versatile Fimbrial Adhesin from Porphyromonas gingivalis

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