Candida Albicans Virulence Factors and Its Pathogenicity

ABSTRACTThe objective of this study was to evaluate whetherCandida albicansexhibits altered pathogenicity characteristics following sublethal antimicrobial photodynamic inactivation (APDI) and if such alterations are maintained in the daughter cells.C. albicanswas exposed to sublethal APDI by using methylene blue (MB) as a photosensitizer (0.05 mM) combined with a GaAlAs diode laser (λ 660 nm, 75 mW/cm2, 9 to 27 J/cm2).In vitro, we evaluated APDI effects onC. albicansgrowth, germ tube formation, sensitivity to oxidative and osmotic stress, cell wall integrity, and fluconazole susceptibility.In vivo, we evaluatedC. albicanspathogenicity with a mouse model of systemic infection. Animal survival was evaluated daily. Sublethal MB-mediated APDI reduced the growth rate and the ability ofC. albicansto form germ tubes compared to untreated cells (P< 0.05). Survival of mice systemically infected withC. albicanspretreated with APDI was significantly increased compared to mice infected with untreated yeast (P< 0.05). APDI increasedC. albicanssensitivity to sodium dodecyl sulfate, caffeine, and hydrogen peroxide. The MIC for fluconazole forC. albicanswas also reduced following sublethal MB-mediated APDI. However, none of those pathogenic parameters was altered in daughter cells ofC. albicanssubmitted to APDI. These data suggest that APDI may inhibit virulence factors and reducein vivopathogenicity ofC. albicans. The absence of alterations in daughter cells indicates that APDI effects are transitory. The MIC reduction for fluconazole following APDI suggests that this antifungal could be combined with APDI to treatC. albicansinfections.

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Does the possession of virulence factor genes mean that those genes will be active?

Journal of Water and Health ◽

10.2166/wh.2009.066 ◽

2009 ◽

Vol 7 (S1) ◽

pp. S19-S28 ◽

Cited By ~ 4

Author(s):

Stephen C. Edberg

Keyword(s):

Public Health ◽

Gastrointestinal Tract ◽

Virulence Factors ◽

Alimentary Tract ◽

The Body ◽

Normal Flora ◽

Mucosal Surfaces ◽

Stomach Acid ◽

Specific Receptors ◽

Virulence Factor Genes

There are a number of relationships the host can establish with the microbes we ingest. For the vast majority of microbes, they have a short-lived liaison with the human host. Either they are destroyed by the stomach acid or bile, or can not establish even a temporary residency in the gastrointestinal tract. Early in life the mucosal surfaces of the body establishes a resident, and generally stable, normal flora. These normal flora microbes, the majority of which are bacteria, have specific receptors for specific areas of the alimentary tract. If the foreign microbe can establish residency, it then may transiently or permanently become part of the normal flora. However, in order to produce disease, it must possess an additional set of virulence factors. While some of these are known, many are not. Those that are known include enzymes, such as protease, lipase, and esterase. Accordingly, VFAR may not be associated with human disease and its presence or absence has no public health meaning.

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Oral candidiasis-adhesion of non-albicans Candida species

Zbornik Matice srpske za prirodne nauke ◽

10.2298/zmspn0814069b ◽

2008 ◽

pp. 69-78 ◽

Cited By ~ 3

Author(s):

Marija Bokor-Bratic

Keyword(s):

Candida Albicans ◽

Candida Species ◽

Oral Candidiasis ◽

Initial Step ◽

Oral Microflora ◽

Mucosal Surfaces ◽

Buccal Epithelial Cells ◽

Mucosal Infection ◽

Denture Acrylics ◽

Candida Colonisation

Oral candidiasis is an opportunistic infection caused primarily by Candida albicans. However, in recent years, species of non-albicans Candida have been implicated more frequently in mucosal infection. Candida species usually reside as commensal organisms and are part of normal oral microflora. Determining exactly how transformation from commensal to pathogen takes place and how it can be prevented is continuous challenge for clinical doctors. Candidal adherence to mucosal surfaces is considered as a critical initial step in the pathogenesis of oral candidiasis. Acrylic dentures, acting as reservoirs, play an important role in increasing the risk from Candida colonisation. Thus, this review discusses what is currently known about the adhesion of non-albicans Candida species of oral origin to buccal epithelial cells and denture acrylics.

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Activation of EphA2-EGFR signaling in oral epithelial cells by Candida albicans virulence factors

PLoS Pathogens ◽

10.1371/journal.ppat.1009221 ◽

2021 ◽

Vol 17 (1) ◽

pp. e1009221

Author(s):

Marc Swidergall ◽

Norma V. Solis ◽

Nicolas Millet ◽

Manning Y. Huang ◽

Jianfeng Lin ◽

...

Keyword(s):

Candida Albicans ◽

Epithelial Cells ◽

Virulence Factors ◽

Growth Factor Receptor ◽

Egfr Signaling ◽

High Concentration ◽

Oral Epithelial Cells ◽

Proinflammatory Mediators ◽

Epidermal Growth ◽

Oral Epithelial

During oropharyngeal candidiasis (OPC), Candida albicans invades and damages oral epithelial cells, which respond by producing proinflammatory mediators that recruit phagocytes to foci of infection. The ephrin type-A receptor 2 (EphA2) detects β-glucan and plays a central role in stimulating epithelial cells to release proinflammatory mediators during OPC. The epidermal growth factor receptor (EGFR) also interacts with C. albicans and is known to be activated by the Als3 adhesin/invasin and the candidalysin pore-forming toxin. Here, we investigated the interactions among EphA2, EGFR, Als3 and candidalysin during OPC. We found that EGFR and EphA2 constitutively associate with each other as part of a heteromeric physical complex and are mutually dependent for C. albicans-induced activation. Als3-mediated endocytosis of a C. albicans hypha leads to the formation of an endocytic vacuole where candidalysin accumulates at high concentration. Thus, Als3 potentiates targeting of candidalysin, and both Als3 and candidalysin are required for C. albicans to cause maximal damage to oral epithelial cells, sustain activation of EphA2 and EGFR, and stimulate pro-inflammatory cytokine and chemokine secretion. In the mouse model of OPC, C. albicans-induced production of CXCL1/KC and CCL20 is dependent on the presence of candidalysin and EGFR, but independent of Als3. The production of IL-1α and IL-17A also requires candidalysin but is independent of Als3 and EGFR. The production of TNFα requires Als1, Als3, and candidalysin. Collectively, these results delineate the complex interplay among host cell receptors EphA2 and EGFR and C. albicans virulence factors Als1, Als3 and candidalysin during the induction of OPC and the resulting oral inflammatory response.

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Virulence Factor and Pathogenicity of Candida albicans in Oral Candidiasis

World Journal of Dentistry ◽

10.5005/jp-journals-10015-1243 ◽

2013 ◽

Vol 4 (4) ◽

pp. 267-271 ◽

Cited By ~ 4

Author(s):

Abdillah Imron Nasution

Keyword(s):

Antibiotic Resistance ◽

Candida Albicans ◽

Immune System ◽

Virulence Factors ◽

Virulence Factor ◽

Oral Candidiasis ◽

Complex Process ◽

Phenotype Switching

ABSTRACT Candida albicans is an opportunistic fungus causing various forms of candidiasis. However, under certain circumstances it is capable of becoming pathogenic. Pathogenicity of oral candidiasis is a complex process and there is no one factor that can be regarded as the direct cause. This review aims to explain the virulence factors of Candida albicans in oral candidiasis infection and its relation to homeostasis in the mouth. Virulence factors of Candida albicans which is closely related to the nature of pathogens include: adherence and coaggregation, interference of immune system, phenotype switching and several supporting factors such as antibiotic resistance and immunomodulating. How to cite this article Nasution AI. Virulence Factor and Pathogenicity of Candida albicans in Oral Candidiasis. World J Dent 2013;4(4):267-271.

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Paeonol assists fluconazole and amphotericin B to inhibit virulence factors and pathogenicity of Candida albicans

Biofouling ◽

10.1080/08927014.2021.1985473 ◽

2021 ◽

pp. 1-16

Author(s):

Min Pan ◽

Qirui Wang ◽

Ting Cheng ◽

Daqiang Wu ◽

Tianming Wang ◽

...

Keyword(s):

Candida Albicans ◽

Amphotericin B ◽

Virulence Factors

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Impact of serial systemic infection on Candida albicans virulence factors

Future Microbiology ◽

10.2217/fmb-2019-0342 ◽

2020 ◽

Vol 15 (13) ◽

pp. 1249-1263

Author(s):

Glaucia S Arita ◽

Daniella R Faria ◽

Karina M Sakita ◽

Franciele AV Rodrigues-Vendramini ◽

Isis RG Capoci ◽

...

Keyword(s):

Candida Albicans ◽

Virulence Factors ◽

Murine Model ◽

Systemic Infection ◽

Systemic Candidiasis ◽

Fungal Burden ◽

Histopathological Findings ◽

Phenotypic Profile ◽

Proteomic Data ◽

Repeated Contact

Aim: To evaluate changes in virulence and pathogenicity approaches from Candida albicans after successive passages in a murine model of systemic candidiasis. Materials & methods: Phenotypic assays were performed using colonies recovered from animals infected serially, totalizing five passages. Results: A progressive infection was observed along the passages, with increased fungal burden and the presence of greater inflammatory areas in the histopathological findings. Recovered strains exhibited increased filamentation and biofilm abilities, along with modulation of phospholipase and proteinase activities. Conclusion: Repeated contact between yeast and host increased the expression of virulence factors. Furthermore, a correspondence between phenotypic profile and proteomic data obtained previously was observed.

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Interactions between Candida albicans and Enterococcus faecalis in an Organotypic Oral Epithelial Model

Microorganisms ◽

10.3390/microorganisms8111771 ◽

2020 ◽

Vol 8 (11) ◽

pp. 1771

Author(s):

Akshaya Lakshmi Krishnamoorthy ◽

Alex A. Lemus ◽

Adline Princy Solomon ◽

Alex M. Valm ◽

Prasanna Neelakantan

Keyword(s):

Candida Albicans ◽

Enterococcus Faecalis ◽

Biofilm Formation ◽

Opportunistic Pathogen ◽

Surface Erosion ◽

Host Immune System ◽

Microbial Invasion ◽

Mucosal Surfaces ◽

Life Threatening ◽

Hyphal Formation

Candida albicans as an opportunistic pathogen exploits the host immune system and causes a variety of life-threatening infections. The polymorphic nature of this fungus gives it tremendous advantage to breach mucosal barriers and cause oral and disseminated infections. Similar to C. albicans, Enterococcus faecalis is a major opportunistic pathogen, which is of critical concern in immunocompromised patients. There is increasing evidence that E. faecalis co-exists with C. albicans in the human body in disease samples. While the interactive profiles between these two organisms have been studied on abiotic substrates and mouse models, studies on their interactions on human oral mucosal surfaces are non-existent. Here, for the first time, we comprehensively characterized the interactive profiles between laboratory and clinical isolates of C. albicans (SC5314 and BF1) and E. faecalis (OG1RF and P52S) on an organotypic oral mucosal model. Our results demonstrated that the dual species biofilms resulted in profound surface erosion and significantly increased microbial invasion into mucosal compartments, compared to either species alone. Notably, several genes of C. albicans involved in tissue adhesion, hyphal formation, fungal invasion, and biofilm formation were significantly upregulated in the presence of E. faecalis. By contrast, E. faecalis genes involved in quorum sensing, biofilm formation, virulence, and mammalian cell invasion were downregulated. This study highlights the synergistic cross-kingdom interactions between E. faecalis and C. albicans in mucosal tissue invasion.

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CX3CR1 Is Dispensable for Control of Mucosal Candida albicans Infections in Mice and Humans

Infection and Immunity ◽

10.1128/iai.02604-14 ◽

2014 ◽

Vol 83 (3) ◽

pp. 958-965 ◽

Cited By ~ 21

Author(s):

Timothy J. Break ◽

Martin Jaeger ◽

Norma V. Solis ◽

Scott G. Filler ◽

Carlos A. Rodriguez ◽

...

Keyword(s):

Candida Albicans ◽

Human Population ◽

Systemic Candidiasis ◽

Gi Tract ◽

Content Type ◽

Commensal Microbiota ◽

Interleukin 17A ◽

Mucosal Surfaces ◽

Bacterial Microbiota ◽

Mucosal Candidiasis

Candida albicansis part of the normal commensal microbiota of mucosal surfaces in a large percentage of the human population. However, perturbations of the host's immune response or bacterial microbiota have been shown to predispose individuals to the development of opportunisticCandidainfections. It was recently discovered that a defect in the chemokine receptor CX3CR1 increases susceptibility of mice and humans to systemic candidiasis. However, whether CX3CR1 confers protection against mucosalC. albicansinfection has not been investigated. Using two different mouse models, we found that Cx3cr1 is dispensable for the induction of interleukin 17A (IL-17A), IL-22, and IL-23 in the tongue after infection, as well as for the clearance of mucosal candidiasis from the tongue or lower gastrointestinal (GI) tract colonization. Furthermore, the dysfunctional human CX3CR1 alleleCX3CR1-M280was not associated with development of recurrent vulvovaginal candidiasis (RVVC) in women. Taken together, these data indicate that CX3CR1 is not essential for protection of the host against mucosal candidiasis, underscoring the dependence on different mammalian immune factors for control of mucosal versus systemicCandidainfections.

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