Yeast Adhesion in the Pathogenesis of Endocarditis Due to Candida albicans: Studies with Adherence-Negative Mutants

Calderone, Richard; Cihlar, R. L.; Lee, D. Dong-Soo; Hoberg, K A; ScheId, W. Michael

doi:10.1093/infdis/152.4.710

Cited by 73 publications

(41 citation statements)

References 14 publications

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“…In addition, they differ from budding white cells in their adhesion to buccal epithelium, cohesion, and hydrophobicity (13). Both secretion and adhesion are potential virulence factors (6,15) which are mediated through the cell wall, and pimples may represent structures which have selectively evolved for one of these types of processes. However, it is difficult to consider how emerging, membrane-bound vesicles would play a role in adhesion or why it would be necessary to encapsulate secretion products in double membranes.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype

1990

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Cells of Candida albicans WO-1 switch frequently and reversibly between two colony-forming phenotypes, white and opaque. In the white form, budding cells appear similar to those of most other strains of C. albicans, but in the opaque form, budding cells are larger, are bean shaped, and possess pimples on the wall. These pimples exhibit a unique and complex morphology. With scanning electron microscopy, a central pit can be discerned, and in many cases, a bleb can be observed emerging from the pimple center. With transmission electron microscopy, channels are evident in some pimples and vesicles are apparent under the pimple in the cytoplasm, in the actual wall of the pimple, or emerging from the tip of the pimple. A large vacuole predominates in the opaque-cell cytoplasm. This vacuole is usually filled with spaghettilike membranous material and in a minority of cases is filled with vesicles, many of which exhibit a relatively uniform size. An antiserum to opaque cells recognizes three opaque-cell-specific antigens with molecular masses of approximately 14.5, 21, and 31 kilodaltons (kDa). Absorption with nonpermeabilized opaque cells demonstrated that only the 14.5-kDa antigen is on the cell surface; indirect immunogold labeling demonstrated that it is localized in or on the pimple. The possibility is suggested that the vacuole of opaque cells is the origin of membrane-bound vesicles which traverse the wall through specialized pimple structures and emerge from the pimple with an intact outer double membrane, a unique phenomenon in yeast cells. The opaque-cell-specific 14.5-kDa antigen either is in the pimple channel or is a component of the emerging vesicle. The functions of the unique opaque-cell pimple and emerging vesicle are not known.Candida albicans and related species are capable of switching at high frequencies between a number of general phenotypes distinguishable by colony morphology (18,20,21,24). There are a number of different switching systems in the species C. albicans and Candida tropicalis, which differ from one another in phenotypic repertoire (18,20,21,26,27). Thus far, all of the systems tested share characteristics of high-and low-frequency modes of switching, heritability, reversibility, a limited number of phenotypes, and stimulation by low doses of UV irradiation (24,25). One of these switching systems, the white-opaque transition, involves a dramatic change not only in colony morphology but also in the basic phenotypes of cells in the budding growth form (1,2,19,21). In the white phase, cells produce smooth white colony domes in all respects similar to those produced by most other strains of C. albicans (2,21 large and sometimes multiple vacuoles (21) as well as unique pimples on the mature cell wall (1, 2). In addition, it has been demonstrated that opaque cells possess one or more opaquecell-specific antigens distributed in the cell wall in a punctate fashion similar to pimple distribution (1, 2).We present here scanning electron microscopy (SEM) and transmission electron microscopy (TE...

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Section: Discussionmentioning

confidence: 99%

Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype

1990

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“…Strains used include C. albicans LAM-1 (N. Deslauriers [41]), LGH 1095 (K. C. Hazen [31]), CA30 (G. T. Cole [25,43]), MYCO177 (Laboratoire de Santé Publique du Québec [LSPQ]), and 4918 (R. A. Calderone [6,44]); C. dubliniensis MYCO1027 (LSPQ [18]), MYCO1181 (LSPQ [18]), MYCO1255 (LSPQ [18]), and MYCO1278 (LSPQ [4,18] Blastoconidia were grown in Sabouraud dextrose broth (Difco Laboratories, Detroit, Mich.) at 25°C for 24 h, or at 30 or 37°C for 18 h, with rotary agitation. The cells were collected by centrifugation and washed twice with 10 mM phosphate-buffered saline (PBS), pH 7.2.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Binding of Candida albicans to Small Intestinal Mucin and Its Role in Adherence to Mucosal Epithelial Cells

et al. 2000

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In order to approximate and adhere to mucosal epithelial cells, Candida must traverse the overlying mucus layer. Interactions of Candida species with mucin and human buccal epithelial cells (BECs) were thus investigated in vitro. Binding of the Candida species to purified small intestinal mucin showed a close correlation with their hierarchy of virulence. Significant differences (P < 0.05) were found among three categories of Candida species adhering highly (C. dubliniensis, C. tropicalis, and C. albicans), moderately (C. parapsilosis and C. lusitaniae) or weakly (C. krusei and C. glabrata) to mucin. Adherence of C. albicans to BECs was quantitatively inhibited by graded concentrations of mucin. However, inhibition of adherence was reversed by pretreatment of mucin with pronase or C. albicans secretory aspartyl proteinase Sap2p but not with sodium periodate. Saturable concentration-and time-dependent binding of mucin to C. albicans was abrogated by pronase or Sap2p treatment of mucin but was unaffected by ␤-mercaptoethanol, sodium periodate, neuraminidase, lectins, or potentially inhibitory sugars. Probing of membrane blots of the mucin with C. albicans revealed binding of the yeast to the 66-kDa cleavage product of the 118-kDa C-terminal glycopeptide of mucin. Although no evidence was found for the participation of C. albicans cell surface mannoproteins in specific receptor-ligand binding to mucin, inhibition of binding by p-nitrophenol (1 mM) and tetramethylurea (0.36 M) revealed that hydrophobic interactions are involved in adherence of C. albicans to mucin. These results suggest that C. albicans may both adhere to and enzymatically degrade mucins by the action of Saps, and that both properties may act to modulate Candida populations in the oral cavity and gastrointestinal tract.

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“…Fig. 2 shows that at the highest doses (1U10 7 , 1U10 6 ) of 1001 all the mice died within a few days. At the lower doses, chronic infection was observed in strains BALB/c and CD2F 1 but not in the susceptible DBA/2 mice, all of which died of an acute infection.…”

Section: Course Of Infection In Balb/c Cd2f 1 and Dba/2 Micementioning

confidence: 97%

“…A number of factors are thought to in£uence the virulence of this fungus [2,3]. Among them are its ability to undergo the dimorphic switch from a budding yeast to a hyphal form [4] and its adhesion capacity [5,6]. Although some strains of C. albicans are partially defective in hyphal development [7^9] or adhesion [10,11] and its virulence has been assayed [9^11], only two mutant strains that fail to form ¢laments in response to serum or other inducers of ¢lamentous growth have been considered avirulent in a mouse infection model [7,8].…”

Section: Introductionmentioning

confidence: 99%

Low virulence of a morphological Candida albicans mutant

Diez-Orejas¹

1999

FEMS Microbiology Letters

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The virulence of Candida albicans 92P, a morphological mutant unable to filament, was assayed in an experimental model of systemic candidiasis in three strains of mice with different susceptibilities to the infection. The mortality parameters studied pointed to the low virulence of this mutant strain. Study of the fungal load of C. albicans 92P in kidneys and brain revealed the presence of low numbers of CFUs and a high percentage of clearance, particularly in the brain. Adhesion studies demonstrated a reduced capability of the mutant to adhere to human epithelial cells. This strain can be considered a potential tool for cloning genes involved in virulence. ß

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Yeast Adhesion in the Pathogenesis of Endocarditis Due to Candida albicans: Studies with Adherence-Negative Mutants

Cited by 73 publications

References 14 publications

Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype

Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype

Characterization of Binding of Candida albicans to Small Intestinal Mucin and Its Role in Adherence to Mucosal Epithelial Cells

Low virulence of a morphological Candida albicans mutant

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