Binding of the periodontitis associated bacterium <i>Porphyromonas gingivalis</i> to glycoproteins from human epithelial cells

Hallén, Ulrika; Björkner, A. E.; Hallberg, Eva

doi:10.1111/j.1399-302x.2008.00437.x

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…Recently, Hallen et al (2008) studied the binding of the periodontitis-associated bacteria P. gingivalis to glycoproteins from human epithelial cells. Glycoconjugate expression on KB cells and in protein preparations was confirmed.…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis fimbriae carbohydrate specificity assessment by glycomics

Sojar

Smith

2012

FEMS Immunol Med Microbiol

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Porphyromonas gingivalis is a major pathogen in adult periodontitis. Fimbriae play an important role in the initial interaction between the bacteria and the host. Our earlier studies suggested that the oligosaccharide moiety of lactoferrin is involved in the interaction with fimbriae. Porphyromonas gingivalis fimbriae bound strongly to albumin-fucosylamide (albumin-1-amido-1-deoxy-L-fucose) and to a lesser extent to albumin-N-acetyl-D-galactosamine (albumin-p-aminophenyl-N-acetyl-β-D-galactosaminide, but failed to bind bovine serum albumin. In this study we explored the glycan array to determine the carbohydrate-binding specificity of P. gingivalis fimbriae. Purified fimbriae bind to glycans which have a Lewis(x), Galβ1-4(Fucα1-3) GlcNAcβ structure in common. Interestingly, all glycans have a terminal fucose moiety and if fucose is removed, the fimbriae fail to bind. This is the first study that suggests that fucose is important for P. gingivalis fimbriae binding.

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Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis fimbriae carbohydrate specificity assessment by glycomics

Sojar

Smith

2012

FEMS Immunol Med Microbiol

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“…These particular sialic acids are expressed on the surface envelope glycoproteins (B, D, and H) of the herpes simplex virion, and these residues are required for viral entry into cells [96]. N-acetyl neuraminic acid is expressed by C. neoformans, is involved in fungal adhesion to macrophages [97], and is also a component of the cell wall of B. burgdorferi [98], while Helicobacter pylori adhesins also bind to this particular form of sialic acid [99,100] as does P. gingivalis [101].…”

Section: Clathrin-mediated Endocytosis (Bin1 Clu Cd2ap Picalm)mentioning

confidence: 99%

Alzheimer′s Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex, C. Pneumoniae, Other Suspect Pathogens, and the Immune System

Carter

2011

International Journal of Alzheimer's Disease

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Alzheimer's disease susceptibility genes, APP and gamma-secretase, are involved in the herpes simplex life cycle, and that of other suspect pathogens (C. pneumoniae, H. pylori, C. neoformans, B. burgdorferri, P. gingivalis) or immune defence. Such pathogens promote beta-amyloid deposition and tau phosphorylation and may thus be causative agents, whose effects are conditioned by genes. The antimicrobial effects of beta-amyloid, the localisation of APP/gamma-secretase in immunocompetent dendritic cells, and gamma secretase cleavage of numerous pathogen receptors suggest that this network is concerned with pathogen disposal, effects which may be abrogated by the presence of beta-amyloid autoantibodies in the elderly. These autoantibodies, as well as those to nerve growth factor and tau, also observed in Alzheimer's disease, may well be antibodies to pathogens, due to homology between human autoantigens and pathogen proteins. NGF or tau antibodies promote beta-amyloid deposition, neurofibrillary tangles, or cholinergic neuronal loss, and, with other autoantibodies, such as anti-ATPase, are potential agents of destruction, whose formation is dictated by sequence homology between pathogen and human proteins, and thus by pathogen strain and human genes. Pathogen elimination in the ageing population and removal of culpable autoantibodies might reduce the incidence and offer hope for a cure in this affliction.

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“…CD33 belongs to an immunoglobulin (Ig)-like family of receptors that are expressed on myeloid cells including microglia [ 53 , 54 ]. CD33 binds to alpha2-3- or alpha2-6-linked sialic acids (N-acetyl neuraminic acid) to which P. gingivalis also binds [ 55 ]. Sialylation of P. gingivalis cell surface components such as LPS may provide additional beneﬁts to this prominent periodontal pathogen in bioﬁlm formation and in escaping complement-mediated killing [ 56 ].…”

Section: Relationship Between P Gingivalis and MImentioning

confidence: 99%

Interaction between genetic factors, Porphyromonas gingivalis and microglia to promote Alzheimer’s disease

Olsen

Singhrao

2020

Journal of Oral Microbiology

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In late-onset Alzheimer disease (AD) pathogenesis, genes, infections and immunity could be significant factors. We have reviewed if the keystone periodontal pathogen Porphyromonas gingivalis may affect genes and microglia (primary immune cells in the brain) to promote AD development. Genes for apolipoprotein, clusterin, CD33, triggering receptor expressed on myeloid cells-2 (TREM-2), tyrosine kinase binding protein (TYR-OBP), and complement receptors can affect microglia. Most of these genes can also be affected by P. gingivalis via its mastering of immune suppression. Besides, P. gingivalis can affect microglia directly in several ways. Taken together, genetic predisposition, P. gingivalis infection and microglia could promote neurodegeneration typical of that reported for AD.

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Binding of the periodontitis associated bacterium Porphyromonas gingivalis to glycoproteins from human epithelial cells

Abstract: These results indicate that carbohydrate structures are involved in the binding process of P. gingivalis to oral epithelial cells and that neuraminic acid plays a significant role in the adhesion process.

Cited by 4 publications

References 26 publications

Porphyromonas gingivalis fimbriae carbohydrate specificity assessment by glycomics

Porphyromonas gingivalis fimbriae carbohydrate specificity assessment by glycomics

Alzheimer′s Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex, C. Pneumoniae, Other Suspect Pathogens, and the Immune System

Interaction between genetic factors, Porphyromonas gingivalis and microglia to promote Alzheimer’s disease

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