Neuraminidase-activated Attachment of Actinomyces naeslundii ATCC 12104 to Human Buccal Epithelial Cells

Saunders, J; Miller, Chris H.

doi:10.1177/00220345830620100501

Cited by 22 publications

(14 citation statements)

References 19 publications

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“…In contrast, a nanH, nanP double mutant had a 53% reduction in its ability to bind to HeLa cells ( Figure 5; Jost et al 2002a, b). These data indicate that the neuraminidases of A. pyogenes play a role in the adherence of this organism to host epithelial cells, probably through exposing cryptic host cell receptors for other A. pyogenes adhesin molecules, as seen with the neuraminidases of S. pneumoniae (Tong et al 1999) and A. viscosus (Saunders and Miller 1983). Lectin-binding studies indicated that the S. pneumoniae NanA neuraminidase-exposed N-acetylglucosamine and D-galactose residues (Tong et al 2002), although the molecular target(s) were not elucidated.…”

Section: Neuraminidasesmentioning

confidence: 77%

Arcanobacterium pyogenes: molecular pathogenesis of an animal opportunist

Jost

Billington

2005

Antonie Van Leeuwenhoek

177

216

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Arcanobacterium pyogenes is a commensal and an opportunistic pathogen of economically important livestock, causing diseases as diverse as mastitis, liver abscessation and pneumonia. This organism possesses a number of virulence factors that contribute to its pathogenic potential. A. pyogenes expresses a cholesterol-dependent cytolysin, pyolysin, which is a haemolysin and is cytolytic for immune cells, including macrophages. Expression of pyolysin is required for virulence and this molecule is the most promising vaccine candidate identified to date. A. pyogenes also possesses a number of adherence mechanisms, including two neuraminidases, the action of which are required for full adhesion to epithelial cells, and several extracellular matrix-binding proteins, including a collagen-binding protein, which may be required for adhesion to collagen-rich tissue. A. pyogenes also expresses fimbriae, which are similar to the type 2 fimbriae of Actinomyces naeslundii, and forms biofilms. However, the role of these factors in the pathogenesis of A. pyogenes infections remains to be elucidated. A. pyogenes also invades and survives within epithelial cells and can survive within J774A.1 macrophages for up to 72 h, suggesting an important role for A. pyogenes interaction with host cells during pathogenesis. The two component regulatory system, PloSR, up-regulates pyolysin expression and biofilm formation but down-regulates expression of proteases, suggesting that it may act as a global regulator of A. pyogenes virulence. A. pyogenes is a versatile pathogen, with an arsenal of virulence determinants. However, most aspects of the pathogenesis of infection caused by this important opportunistic pathogen remain poorly characterized.

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Section: Neuraminidasesmentioning

confidence: 77%

Arcanobacterium pyogenes: molecular pathogenesis of an animal opportunist

Jost

Billington

2005

Antonie Van Leeuwenhoek

177

216

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“…Neuraminidase decreases the viscosity of the lung mucus, which may predispose individuals to secondary pneumonia by many of the pathogens listed in Table 2. The purified enzyme in vitro increases the adhesion of oral bacteria to human buccal epithelial cells (47,48 …”

Section: Resultsmentioning

confidence: 99%

Many pulmonary pathogenic bacteria bind specifically to the carbohydrate sequence GalNAc beta 1-4Gal found in some glycolipids.

Krivan

Roberts

Ginsburg

1988

Proc. Natl. Acad. Sci. U.S.A.

379

351

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Pneumonia is one of the most common causes of death from infectious disease in the United States. To examine the possible role of carbohydrates as adhesion receptors for infection, several pulmonary pathogenic bacteria were studied for binding to glycosphingolipids. Radiolabeled bacteria were layered on thin-layer chromatograms of separated glycosphingolipids, and bound bacteria were detected by autoradiography. The classic triad of infectious bacteria found in cystic fibrosis, Pseudomonas aeruginosa, Haemophilus influenzae, and Staphylococcus aureus, along with other bacteria commonly implicated in typical pneumonia, such as Streptococcus pneumoniae, Kiebsiella pneumoniae, and certain Escherichia coli, bind specifically to fucosylasialo-GM1 (Fucal-2Galfl1-3GalNAcI81-4GalIl1-4GlcI31-lCer), asialo-GM1

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“…Type 2 fimbriae are known to be involved in coaggregation with many S. sanguis and S. mitis strains and in attachment to buc cal epithelial cells, but are not involved in adherence to experimental salivary pelli cle, as has been shown for type I fimbriae [Saunders and Miller, 1980;Cisar et al" 1984b;Brennan et al, 1984;Clark, 1985]. If 2-hour plaque can be interpreted to re present initial adherence, the similar pro portions of A. naeslundii and A. viscosus could be hypothesized to be partly due to coaggregation between S. sanguis and A. naeslundii.…”

Section: Discussionmentioning

confidence: 99%

In vivo Colonization of Salivary Pellicle by Haemophilus, Actinomyces and Streptococcus Species

Liljemark¹,

Fenner²,

Bloomquist³

1986

Caries Res

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Eight human subjects with healthy oral conditions were examined to study developing dental plaque. Supragingival plaque, buccal mucosa, tongue dorsum and saliva were sampled prior to the pumicing and cleaning of facial surfaces of the four upper premolars and two first molars. Samples were processed anaerobically on media that were selective for the oral Streptococcus spp., Haemophilus spp., and Actinomyces spp., as well as supplemented blood agar for identification of gram-negative bacterial groups and total cultivable flora. NAD-requiring Haemophilus spp., Streptococcus sanguis, Streptococcus mitis, Streptococcus mutans and Streptococcus salivarius were found in most oral samples. Analysis of the distribution of the Actinomyces spp., Actinomyces viscosus, Actinomyces naeslundii and Actinomyces odontolyticus in oral samples prior to teeth cleaning, found no significant differences between proportions or prevalence of these species in saliva, buccal mucosa, tongue, or pooled plaque samples. All three species were found on most surfaces in all subjects. Following cleaning, plaque was allowed to develop for 48 h. Proportions of a species in 2-hour plaque, when higher than proportions in the same individual’s saliva samples, were interpreted to be due to a species promotion by salivary pellicle (as 2-hour plaque from cleaned teeth). A median ratio of 1:3 of saliva versus 2-hour plaque was seen for A. odontolyticus suggesting some promotion by pellicle. A. viscosus and S. sanguis showed median ratios of saliva:2-hour plaque of 1:6 or higher, suggesting that salivary pellicle strongly promoted these species’ adherence. Developing plaques contained high proportions of streptococci, especially S. sanguis and S. mitis, as well as Haemophilus parainfluenzae. Significant increases were seen in proportions of S. sanguis in 48-hour versus 24-hour, and 2-hour plaques. A. viscosus, A. naeslundii and A. odontolyticus were found in most developing plaque samples and in similar proportions to each other. A significant twofold increase in proportions of A. odontolyticus, and fourfold increase of S. sanguis, was seen in 48- versus 2-hour plaques suggesting growth of these species. Forty-eight-hour plaque was composed primarily of Facklam type 1 S. sanguis and this species was found in significantly higher proportions than S. salivarius or S. mutans. NAD-requiring haemophili were found in high proportions and comprised 99% of the haemophili in 48-hour plaque. Although A. naeslundii was not dectected in as many 48-hour samples as A. viscosus or A. odontolyticus, these three species were found in similar proportions in 48-hour developing plaque samples.

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Neuraminidase-activated Attachment of Actinomyces naeslundii ATCC 12104 to Human Buccal Epithelial Cells

Cited by 22 publications

References 19 publications

Arcanobacterium pyogenes: molecular pathogenesis of an animal opportunist

Arcanobacterium pyogenes: molecular pathogenesis of an animal opportunist

Many pulmonary pathogenic bacteria bind specifically to the carbohydrate sequence GalNAc beta 1-4Gal found in some glycolipids.

In vivo Colonization of Salivary Pellicle by Haemophilus, Actinomyces and Streptococcus Species

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