Identification of salivary basic proline-rich proteins as receptors for Candida albicans adhesion

O’Sullivan, Justin M.; Cannon, Richard D.; Sullivan, Patrick A.; Jenkinson, Howard F.

doi:10.1099/00221287-143-2-341

Cited by 43 publications

(37 citation statements)

References 43 publications

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“…These observations agree with previous studies which show that C. albicans adherence to hydroxyapatite is greatly stimulated when it is coated with either whole or parotid saliva compared to its adherence to hydrated uncoated HA beads (10,11). There are indications that C. albicans adhesins may recognize basic proline-rich proteins in the pellicle (43). However, the identity of the cell wall protein and the type of adhesion receptor interactions remain to be elucidated.…”

Section: Vol 77 2011 Role Of Gtfb In C Albicans-s Mutans Interactsupporting

confidence: 91%

Role of Glucosyltransferase B in Interactions of Candida albicans with Streptococcus mutans and with an Experimental Pellicle on Hydroxyapatite Surfaces

Gregoire

Xiao

Silva

et al. 2011

Appl Environ Microbiol

167

218

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Candida albicans and mutans streptococci are frequently detected in dental plaque biofilms from toddlers afflicted with early childhood caries. Glucosyltransferases (Gtfs) secreted by Streptococcus mutans bind to saliva-coated apatite (sHA) and to bacterial surfaces, synthesizing exopolymers in situ, which promote cell clustering and adherence to tooth enamel. We investigated the potential role Gtfs may play in mediating the interactions between C. albicans SC5314 and S. mutans UA159, both with each other and with the sHA surface. GtfB adhered effectively to the C. albicans yeast cell surface in an enzymatically active form, as determined by scintillation spectroscopy and fluorescence imaging. The glucans formed on the yeast cell surface were more susceptible to dextranase than those synthesized in solution or on sHA and bacterial cell surfaces (P < 0.05), indicating an elevated ␣-1,6-linked glucose content. Fluorescence imaging revealed that larger numbers of S. mutans cells bound to C. albicans cells with glucans present on their surface than to yeast cells without surface glucans (uncoated). The glucans formed in situ also enhanced C. albicans interactions with sHA, as determined by a novel single-cell micromechanical method. Furthermore, the presence of glucan-coated yeast cells significantly increased the accumulation of S. mutans on the sHA surface (versus S. mutans incubated alone or mixed with uncoated C. albicans; P < 0.05). These data reveal a novel cross-kingdom interaction that is mediated by bacterial GtfB, which readily attaches to the yeast cell surface. Surface-bound GtfB promotes the formation of a glucan-rich matrix in situ and may enhance the accumulation of S. mutans on the tooth enamel surface, thereby modulating the development of virulent biofilms.

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Section: Vol 77 2011 Role Of Gtfb In C Albicans-s Mutans Interactsupporting

confidence: 91%

Role of Glucosyltransferase B in Interactions of Candida albicans with Streptococcus mutans and with an Experimental Pellicle on Hydroxyapatite Surfaces

Gregoire

Xiao

Silva

et al. 2011

Appl Environ Microbiol

167

218

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“…91 In many cases the adhesion of C. albicans to oral surfaces is promoted by saliva adsorbed either to the yeast or to the oral surface as a pellicle. 89,90,92,93 Adhesion of C. albicans to oral surfaces is mediated by cell-surface adhesins, which are often mannoproteins. Well-characterized adhesions implicated in biofi lm formation include Hwp1p (hyphal wall protein) 94 and Als (agglutinin-like sequence) family members such as Als3p.…”

Section: Oral Biofi Lms and Antifungal Drug Resistancementioning

confidence: 99%

Antifungal drug resistance of oral fungi

2010

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Fungi comprise a minor component of the oral microbiota but give rise to oral disease in a significant proportion of the population. The most common form of oral fungal disease is oral candidiasis, which has a number of presentations. The mainstay for the treatment of oral candidiasis is the use of polyenes, such as nystatin and amphotericin B, and azoles including miconazole, fluconazole, and itraconazole. Resistance of fungi to polyenes is rare, but some Candida species, such as Candida glabrata and C. krusei, are innately less susceptible to azoles, and C. albicans can acquire azole resistance. The main mechanism of high-level fungal azole resistance, measured in vitro, is energy-dependent drug efflux. Most fungi in the oral cavity, however, are present in multispecies biofilms that typically demonstrate an antifungal resistance phenotype. This resistance is the result of multiple factors including the expression of efflux pumps in the fungal cell membrane, biofilm matrix permeability, and a stress response in the fungal cell. Removal of dental biofilms, or treatments to prevent biofilm development in combination with antifungal drugs, may enable better treatment and prevention of oral fungal disease.

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“…In order to identify the saliva proteins to which C. albicans cells adhere, investigators have developed blot overlay assays (Newman et al, 1996;O'Sullivan et al, 1997), in which saliva proteins are separated by SDS polyacrylamide gel electrophoresis, electroblotted onto nitrocellulose membranes, and incubated with either radiolabeled (O or fluorescently labeled (Newman et al, 1996) and Psi (Newman et al, 1996), as receptors for C. albicans adhesion.…”

Section: Removalmentioning

confidence: 99%

Oral Colonization By Candida Albicans

Cannon

Chaffin

1999

Critical Reviews in Oral Biology & Medicine

276

193

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Candida albicans is a commensal yeast normally present in small numbers in the oral flora of a large proportion of humans. Colonization of the oral cavity by C. albicans involves the acquisition and maintenance of a stable yeast population. Micro-organisms are continually being removed from the oral cavity by host clearance mechanisms, and so, in order to survive and inhabit this eco-system, C. albicans cells have to adhere and replicate. The oral cavity presents many niches for C. albicans colonization, and the yeast is able to adhere to a plethora of ligands. These include epithelial and bacterial cell-surface molecules, extracellular matrix proteins, and dental acrylic. In addition, saliva molecules, including basic proline-rich proteins, adsorbed to many oral surfaces promote C. albicans adherence. Several adhesins present in the C. albicans cell wall have now been partially characterized. Adherence involves lectin, protein-protein, and hydrophobic interactions. As C. albicans cells evade host defenses and colonize new environments by penetrating tissues, they are exposed to new adherence receptors and respond by expressing alternative adhesins. The relatively small number of commensal Candida cells in the oral flora raises the possibility that strategies can be devised to prevent oral colonization and infection. However, the variety of oral niches and the complex adherence mechanisms of the yeast mean that such a goal will remain elusive until more is known about the contribution of each mechanism to colonization.

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Identification of salivary basic proline-rich proteins as receptors for Candida albicans adhesion

Cited by 43 publications

References 43 publications

Role of Glucosyltransferase B in Interactions of Candida albicans with Streptococcus mutans and with an Experimental Pellicle on Hydroxyapatite Surfaces

Role of Glucosyltransferase B in Interactions of Candida albicans with Streptococcus mutans and with an Experimental Pellicle on Hydroxyapatite Surfaces

Antifungal drug resistance of oral fungi

Oral Colonization By Candida Albicans

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