scholarly journals Early Adhesion of Candida albicans onto Dental Acrylic Surfaces

2017 ◽  
Vol 96 (8) ◽  
pp. 917-923 ◽  
Author(s):  
S. Aguayo ◽  
H. Marshall ◽  
J. Pratten ◽  
D. Bradshaw ◽  
J.S. Brown ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Clinical Isolate ◽  
Force Spectroscopy ◽  
Laboratory Strain ◽  
Culture Conditions ◽  
The Body ◽  
Yeast Cells ◽  
Adhesion Forces ◽  
Reliable Technique ◽  
Mother Cells

Denture-associated stomatitis is a common candidal infection that may give rise to painful oral symptoms, as well as be a reservoir for infection at other sites of the body. As poly (methyl methacrylate) (PMMA) remains the main material employed in the fabrication of dentures, the aim of this research was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing an atomic force microscopy (AFM) single-cell force spectroscopy (SCFS) technique. For experiments, tipless AFM cantilevers were functionalized with PMMA microspheres and probed against C. albicans cells immobilized onto biopolymer-coated substrates. Both a laboratory strain and a clinical isolate of C. albicans were used for SCFS experiments. Scanning electron microscopy (SEM) and AFM imaging of C. albicans confirmed the polymorphic behavior of both strains, which was dependent on growth culture conditions. AFM force-spectroscopy results showed that the adhesion of C. albicans to PMMA is morphology dependent, as hyphal tubes had increased adhesion compared with yeast cells ( P < 0.05). C. albicans budding mother cells were found to be nonadherent, which contrasts with the increased adhesion observed in the tube region. Comparison between strains demonstrated increased adhesion forces for a clinical isolate compared with the lab strain. The clinical isolate also had increased survival in blood and reduced sensitivity to complement opsonization, providing additional evidence of strain-dependent differences in Candida-host interactions that may affect virulence. In conclusion, PMMA-modified AFM probes have shown to be a reliable technique to characterize the adhesion of C. albicans to acrylic surfaces.

scholarly journals Identification of a Cell Death Pathway in Candida albicans during the Response to Pheromone

2010 ◽  
Vol 9 (11) ◽  
pp. 1690-1701 ◽  
Author(s):  
Kevin Alby ◽  
Dana Schaefer ◽  
Racquel Kim Sherwood ◽  
Stephen K. Jones ◽  
Richard J. Bennett
Keyword(s):  
Cell Death ◽  
Candida Albicans ◽  
Laboratory Strain ◽  
Opportunistic Pathogen ◽  
Cell Types ◽  
Yeast Cells ◽  
Phenotypic Switching ◽  
Morphological Response ◽  
Content Type ◽  
Cell Death Pathway

ABSTRACT Mating in hemiascomycete yeasts involves the secretion of pheromones that induce sexual differentiation in cells of the opposite mating type. Studies in Saccharomyces cerevisiae have revealed that a subpopulation of cells experiences cell death during exposure to pheromone. In this work, we tested whether the phenomenon of pheromone-induced death (PID) also occurs in the opportunistic pathogen Candida albicans. Mating in C. albicans is uniquely regulated by white-opaque phenotypic switching; both cell types respond to pheromone, but only opaque cells undergo the morphological transition and cell conjugation. We show that approximately 20% of opaque cells, but not white cells, of laboratory strain SC5314 experience pheromone-induced death. Furthermore, analysis of mutant strains revealed that PID was significantly reduced in strains lacking Fig1 or Fus1 transmembrane proteins that are induced during the mating process and, we now show, are necessary for efficient mating in C. albicans. The level of PID was also Ca2+ dependent, as chelation of Ca2+ ions increased cell death to almost 50% of the population. However, in contrast to S. cerevisiae PID, pheromone-induced killing of C. albicans cells was largely independent of signaling via the Ca2+-dependent protein phosphatase calcineurin, even when combined with the loss of Cmk1 and Cmk2 proteins. Finally, we demonstrate that levels of PID vary widely between clinical isolates of C. albicans, with some strains experiencing close to 70% cell death. We discuss these findings in light of the role of prodeath and prosurvival pathways operating in yeast cells undergoing the morphological response to pheromone.

scholarly journals Quantification of the Adhesion Strength of Candida albicans to Tooth Enamel

2021 ◽  
Vol 9 (11) ◽  
pp. 2213
Author(s):  
Gubesh Gunaratnam ◽  
Johanna Dudek ◽  
Philipp Jung ◽  
Sören L. Becker ◽  
Karin Jacobs ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Adhesion Strength ◽  
Adhesion Force ◽  
Tooth Enamel ◽  
Opportunistic Pathogen ◽  
Enamel Surface ◽  
Yeast Cells ◽  
Adhesion Forces ◽  
Initial Adhesion ◽  
Salivary Pellicle

Caries is one of the most prevalent diseases worldwide, which is caused by the degradation of the tooth enamel surface. In earlier research the opportunistic pathogen Candida albicans has been associated with the formation of caries in children. Colonization of teeth by C. albicans starts with the initial adhesion of individual yeast cells to the tooth enamel surface. In this study, we visualized the initial colonization of C. albicans yeast cells on pellicle-covered enamel by scanning electron microscopy. To quantitatively unravel the initial adhesion strength, we applied fluidic force microscopy-based single-cell force spectroscopy to examine the key adhesion parameters adhesion force, rupture length and de-adhesion work. We analyzed single saliva-treated or untreated yeast cells on tooth enamel specimens with or without salivary pellicle. Under all tested conditions, adhesion forces in the lower nanonewton range were determined. Furthermore, we have found that all adhesion parameters were enhanced on the pellicle-covered compared to the uncovered enamel. Our data suggest that initial adhesion occurs through a strong interaction between yeast cell wall-associated adhesins and the salivary pellicle. Future SCFS studies may show whether specific management of the salivary pellicle reduces the adhesion of C. albicans on teeth and thus contributes to caries prophylaxis.

Ultrastructure of Candida Albicans And Saccharomyces Cerevisiae After Treatment With Sch 56301 (An Aureobasidin)

1999 ◽  
Vol 5 (S2) ◽  
pp. 1276-1277
Author(s):  
B.J. Dovey-Hartman ◽  
C. Cramer ◽  
J. Greene ◽  
K.J. Shaw ◽  
R.S. Hare ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Wall ◽  
Candida Albicans ◽  
Yeast Cells ◽  
Cyclic Depsipeptide ◽  
Spindle Elongation ◽  
Mother Cells ◽  
Cell Changes ◽  
Normal Cell Cycle

Aureobasidins are cyclic depsipeptide natural products that have been shown to be fungicidal against a wide variety of fungi. We have studied the effect of an aureobasidin-like compound, SCH 56301 on the morphology and cytology of yeast cells. For both, Candida albicans and Saccharomyces cerevisiae, the normal cell cycle is disrupted by sub-lethal concentrations of the compound. In Saccharomyces, cells accumulate at the G2/M border of the cell cycle, DNA replication is essentially complete and a short nuclear spindle is visible; however, nuclear migration and spindle elongation do not occur and consequently a small round daughter cell remains attached to the mother cell. Changes in cell wall morphology are visible at old bud scars remaining on mother cells. Under the conditions of preparation of the specimens, there may have been insufficient cross-linking during treatment with SCH 56301 so that intracellular pressure appears to be pushing on a weakened cell wall at these points.

Pathogenicity of Candida tropicalis and Candida albicans after gastrointestinal inoculation in mice

1980 ◽  
Vol 29 (2) ◽  
pp. 808-813 ◽  
Author(s):  
J R Wingard ◽  
J D Dick ◽  
W G Merz ◽  
G R Sandford ◽  
R Saral ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Mouse Model ◽  
Lung Tissue ◽  
Candida Tropicalis ◽  
Cytotoxic Drugs ◽  
Clinical Isolates ◽  
Yeast Cells ◽  
Gastrointestinal Mucosa ◽  
Compromised Host ◽  
Adult Mice

The ability of clinical isolates of Candida albicans and candida tropicalis to invade through normal and damaged gastrointestinal mucosa was determined. Adult mice were treated with either gentamicin or gentamicin and cytarabine. Suspensions of yeast cells (10(7)) were administered through a catheter intraesophageally. Invasion was determined by culturing liver, kidney, and lung tissue from mice sacrificed after 48 h. C. albicans and C. tropicalis were incapable of invading through normal gastrointestinal mucosa in mice treated only with gentamicin. Two isolates of C. tropicalis penetrated the damaged gastrointestinal mucosa in 69% (49 of 71) of mice treated with gentamicin and cytarabine. In contrast, three isolates of C. albicans penetrated he damaged gastrointestinal mucosa in only 23% (14 of 62) of mice. These results suggest that C. tropicalis is more capable of invading through damaged gastrointestinal mucosa than C. albicans. The observations in this mouse model parallel those seen in patients on cytotoxic drugs. Therefore, this model offers a tool for investigation of the pathogenicity of these organisms in a model analogous to the compromised host.

scholarly journals Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β

2018 ◽  
Vol 19 (11) ◽  
pp. 3672 ◽  
Author(s):  
Yutaro Tsubakihara ◽  
Aristidis Moustakas
Keyword(s):  
Growth Factor ◽  
Tumor Cells ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Basement Membranes ◽  
The Body ◽  
Common Denominator ◽  
Adhesion Forces ◽  
Mesenchymal Transition

Metastasis of tumor cells from primary sites of malignancy to neighboring stromal tissue or distant localities entails in several instances, but not in every case, the epithelial-mesenchymal transition (EMT). EMT weakens the strong adhesion forces between differentiated epithelial cells so that carcinoma cells can achieve solitary or collective motility, which makes the EMT an intuitive mechanism for the initiation of tumor metastasis. EMT initiates after primary oncogenic events lead to secondary secretion of cytokines. The interaction between tumor-secreted cytokines and oncogenic stimuli facilitates EMT progression. A classic case of this mechanism is the cooperation between oncogenic Ras and the transforming growth factor β (TGFβ). The power of TGFβ to mediate EMT during metastasis depends on versatile signaling crosstalk and on the regulation of successive waves of expression of many other cytokines and the progressive remodeling of the extracellular matrix that facilitates motility through basement membranes. Since metastasis involves many organs in the body, whereas EMT affects carcinoma cell differentiation locally, it has frequently been debated whether EMT truly contributes to metastasis. Despite controversies, studies of circulating tumor cells, studies of acquired chemoresistance by metastatic cells, and several (but not all) metastatic animal models, support a link between EMT and metastasis, with TGFβ, often being a common denominator in this link. This article aims at discussing mechanistic cases where TGFβ signaling and EMT facilitate tumor cell dissemination.

Nanoscale adhesion forces between the fungal pathogen Candida albicans and macrophages

2016 ◽  
Vol 1 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Sofiane El-Kirat-Chatel ◽  
Yves F. Dufrêne
Keyword(s):  
Atomic Force Microscopy ◽  
Candida Albicans ◽  
Immune Cells ◽  
Fungal Pathogen ◽  
Fungal Pathogens ◽  
Adhesion Forces ◽  
Force Microscopy ◽  
Atomic Force

We establish atomic force microscopy as a new nanoscopy platform for quantifying the forces between fungal pathogens and immune cells.

scholarly journals Photodynamic Effect of 5,10,15,20-Tetrakis[4-(3-N,N-dimethylaminopropoxy)phenyl]chlorin towards the Human Pathogen Candida albicans under Different Culture Conditions

Photochem ◽  
2021 ◽  
Vol 1 (3) ◽  
pp. 505-522
Author(s):  
Paula V. Cordero ◽  
Darío D. Ferreyra ◽  
María E. Pérez ◽  
María G. Alvarez ◽  
Edgardo N. Durantini
Keyword(s):  
Candida Albicans ◽  
Culture Conditions ◽  
Oxygen Species ◽  
Type Ii ◽  
Planktonic Cells ◽  
Quenching Rate ◽  
Log Reduction ◽  
Quenching Rate Constant ◽  
Bimolecular Quenching ◽  
Human Pathogen Candida Albicans

Photocytotoxic activity sensitized by 5,10,15,20-tetrakis[4-(3-N,N-dimethylaminopropoxy)phenyl]chlorin (TAPC) was investigated in Candida albicans under different culture conditions. Planktonic cells incubated with 2.5 μM TAPC were eradicated after 5 min irradiation with white light. Studies in the presence of reactive oxygen species scavengers indicated the involvement of mainly a type II mechanism. Furthermore, cell growth of C. albicans was suppressed in the presence of 5 μM TAPC. A decrease in pseudohyphae survival of 5 log was found after 30 min irradiation. However, the photokilling of this virulence factor reached a 1.5 log reduction in human serum. The uptake of TAPC by pseudohyphae decreased in serum due to the interaction of TAPC with albumin. The binding constant of the TAPC-albumin complex was ~104 M−1, while the bimolecular quenching rate constant was ~1012 s−1 M−1, indicating that this process occurred through a static process. Thus, the photoinactivation of C. albicans was considerably decreased in the presence of albumin. A reduction of 2 log in cell survival was observed using 4.5% albumin and 30 min irradiation. The results allow optimizing the best conditions to inactivate C. albicans under different culture conditions.

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