Candida albicans

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Strain details

Name	Provider name	Provider's strain ID	Genotypes	Phenotypes	Synonym	Comments	Based on

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Showing 5 out of a possible 18 Programmes Advanced Programmes list for this Organism with search and filtering

Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

The yeast Candida albicans and the filamentous fungus Aspergillus fumigatus are by far the most important causes of life-threatening invasive mycoses in Europe. Despite the increasing incidence of these infections, the current diagnosis is still difficult and often too late, and options for therapies are limited. Moreover, A. fumigatus and C. albicans have developed multiple sophisticated, specific and unique pathogenicity mechanisms. Many of these mechanisms are not well understood. Research on ...

Projects: FungiNet total, FungiNet A - Aspergillus projects, FungiNet B - Bioinformatics projects, FungiNet C - Candida projects, INF, A1, A2, A3, A4 (E), A5, B1, B2, B3 (E), B4, C1, C2, C3, C4 (E), C5, C6 (E), Z2, Z1, B5, A6, A7, A8, C7

Web page: http://www.funginet.de/home.html

Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Web page: http://www.funginet.de/home.html

Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Web page: http://www.funginet.de/home.html

Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Web page: http://www.funginet.de/home.html

Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Web page: http://www.funginet.de/home.html

View all 18 Programmes

Showing 5 out of a possible 18 Projects Advanced Projects list for this Organism with search and filtering

INF

Integrated database for experimental data

Within the Collaborative Research Center / Transregio 124 “Pathogenic fungi and their human host: Networks of Interaction – FungiNet”, the INF project is responsible to analyse and share OMICS data. Databases help to foster the collaboration within FungiNet as an important point of the Collaborative Research Center. Therefore, we set-up two databases:

a) SEEK is a web-based platform to find, share and exchange unstructured data and knowledge, such as ...

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-inf.html

Organisms: Aspergillus fumigatus, Candida albicans

FungiNet total

No description specified

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/home.html

Organisms: Aspergillus fumigatus, Candida albicans

Ionic regulation of Th17-mediated immune responses to Candida infection

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: https://www.funginet.de/project-c7.html

Organisms: Candida albicans

C4 (E)

Mechanisms of adhesion and modulation of human immune cells by Candida albicans

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-c4.html

Organisms: Candida albicans

C6 (E)

Role of secreted Candida albicans proteins in immune evasion and pathogenicity

Programme: Collaborative Research Center / Transregio 124 "Pathogenic fungi and their human host: Networks of Interaction - FungiNet"

Public web page: http://www.funginet.de/project-c6.html

Organisms: Candida albicans

View all 18 Projects

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Advanced Models list for this Organism with search and filtering

State-based model of whole-blood infection assay with PMN-mediated immune evasion mechanism

This model is a variant of the previously developed SBM of whole-blood infection assay. While in the previous model a spontaneous immune evasion mechanism (A) was implemented in this model immune evasion was caused by PMN molecule secretion (B).

Creators: Teresa Lehnert, Maria T. E. Prauße

Submitter: Sandra Timme

Model type: Not specified

Model format: Not specified

Environment: Not specified

Organism: Candida albicans

Investigations: No Investigations

Studies: No Studies

Assays: No Assays

Created: 18th Feb 2021 at 09:28

State-based model of whole-blood infection assays with Candida albicans

The state-based model (SBM) allow to simulate the interplay between innate immune cells, such as monocytes and PMN, and Candida albicans and to quantify immune reaction rates like phagocytosis and killing rates. It is implemented in C++.

Creator: Teresa Lehnert

Submitter: Sandra Timme

Model type: Not specified

Model format: Not specified

Environment: Not specified

Organism: Candida albicans

Investigations: No Investigations

Studies: No Studies

Assays: No Assays

Created: 18th Feb 2021 at 09:23, Last updated: 18th Feb 2021 at 09:23

DynaCoSys

DynaCoSys models the complement system by using a combination of Ordinary and Partial Differential Equations.

Creators: Teresa Lehnert, Alexander Tille

Submitter: Sandra Timme

Model type: Partial differential equations (PDE)

Model format: Not specified

Environment: Not specified

Organism: Candida albicans

Investigations: No Investigations

Studies: No Studies

Assays: No Assays

Created: 16th Feb 2021 at 16:25, Last updated: 18th Feb 2021 at 09:00

6 hidden items

Showing 5 out of a possible 14 Publications Advanced Publications list for this Organism with search and filtering

Quantification of Factor H Mediated Self vs. Non-self Discrimination by Mathematical Modeling.

FungiNet C - Candida projects, B4

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Abstract (Expand)

The complement system is part of the innate immune system and plays an important role in the host defense against infectious pathogens. One of the main effects is the opsonization of foreign invaders … and subsequent uptake by phagocytosis. Due to the continuous default basal level of active complement molecules, a tight regulation is required to protect the body's own cells (self cells) from opsonization and from complement damage. A major complement regulator is Factor H, which is recruited from the fluid phase and attaches to cell surfaces where it effectively controls complement activation. Besides self cells, pathogens also have the ability to bind Factor H; they can thus escape opsonization and phagocytosis causing severe infections. In order to advance our understanding of the opsonization process at a quantitative level, we developed a mathematical model for the dynamics of the complement system-termed DynaCoSys model-that is based on ordinary differential equations for cell surface-bound molecules and on partial differential equations for concentration profiles of the fluid phase molecules in the environment of cells. This hybrid differential equation approach allows to model the complement cascade focusing on the role of active C3b in the fluid phase and on the cell surface as well as on its inactivation on the cell surface. The DynaCoSys model enables us to quantitatively predict the conditions under which Factor H mediated complement evasion occurs. Furthermore, investigating the quantitative impact of model parameters by a sensitivity analysis, we identify the driving processes of complement activation and regulation in both the self and non-self regime. The two regimes are defined by a critical Factor H concentration on the cell surface and we use the model to investigate the differential impact of complement model parameters on this threshold value. The dynamic modeling on the surface of pathogens are further relevant to understand pathophysiological situations where Factor H mutants and defective Factor H binding to target surfaces results in pathophysiology such as renal and retinal disease. In the future, this DynaCoSys model will be extended to also enable evaluating treatment strategies of complement-related diseases.

Authors: A. Tille, T. Lehnert, P. F. Zipfel, M. T. Figge

Date Published: 5th Oct 2020

Publication Type: Not specified

PubMed ID: 33013842

Citation: Front Immunol. 2020 Sep 2;11:1911. doi: 10.3389/fimmu.2020.01911. eCollection 2020.

Created: 16th Feb 2021 at 16:08, Last updated: 17th Jan 2024 at 10:24

Quantitative Simulations Predict Treatment Strategies Against Fungal Infections in Virtual Neutropenic Patients.

FungiNet C - Candida projects, B4

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Abstract (Expand)

The condition of neutropenia, i.e., a reduced absolute neutrophil count in blood, constitutes a major risk factor for severe infections in the affected patients. Candida albicans and Candida glabrata …

Authors: S. Timme, T. Lehnert, M. T. E. Prausse, K. Hunniger, I. Leonhardt, O. Kurzai, M. T. Figge

Date Published: 20th Apr 2018

Publication Type: Not specified

PubMed ID: 29670632

Citation: Front Immunol. 2018 Apr 4;9:667. doi: 10.3389/fimmu.2018.00667. eCollection 2018.

Created: 11th Feb 2021 at 15:43, Last updated: 17th Jan 2024 at 10:24

Predictive Virtual Infection Modeling of Fungal Immune Evasion in Human Whole Blood.

FungiNet C - Candida projects, B4

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Abstract (Expand)

Bloodstream infections by the human-pathogenic fungi Candida albicans and Candida glabrata increasingly occur in hospitalized patients and are associated with high mortality rates. The early immune … response against these fungi in human blood comprises a concerted action of humoral and cellular components of the innate immune system. Upon entering the blood, the majority of fungal cells will be eliminated by innate immune cells, i.e., neutrophils and monocytes. However, recent studies identified a population of fungal cells that can evade the immune response and thereby may disseminate and cause organ dissemination, which is frequently observed during candidemia. In this study, we investigate the so far unresolved mechanism of fungal immune evasion in human whole blood by testing hypotheses with the help of mathematical modeling. We use a previously established state-based virtual infection model for whole-blood infection with C. albicans to quantify the immune response and identified the fungal immune-evasion mechanism. While this process was assumed to be spontaneous in the previous model, we now hypothesize that the immune-evasion process is mediated by host factors and incorporate such a mechanism in the model. In particular, we propose, based on previous studies that the fungal immune-evasion mechanism could possibly arise through modification of the fungal surface by as of yet unknown proteins that are assumed to be secreted by activated neutrophils. To validate or reject any of the immune-evasion mechanisms, we compared the simulation of both immune-evasion models for different infection scenarios, i.e., infection of whole blood with either C. albicans or C. glabrata under non-neutropenic and neutropenic conditions. We found that under non-neutropenic conditions, both immune-evasion models fit the experimental data from whole-blood infection with C. albicans and C. glabrata. However, differences between the immune-evasion models could be observed for the infection outcome under neutropenic conditions with respect to the distribution of fungal cells across the immune cells. Based on these predictions, we suggested specific experimental studies that might allow for the validation or rejection of the proposed immune-evasion mechanism.

Authors: M. T. E. Prausse, T. Lehnert, S. Timme, K. Hunniger, I. Leonhardt, O. Kurzai, M. T. Figge

Date Published: 6th Apr 2018

Publication Type: Not specified

PubMed ID: 29619027

Citation: Front Immunol. 2018 Mar 21;9:560. doi: 10.3389/fimmu.2018.00560. eCollection 2018.

Created: 11th Feb 2021 at 15:53, Last updated: 17th Jan 2024 at 10:24

N-Acetylglucosamine-Induced Cell Death in Candida albicans and Its Implications for Adaptive Mechanisms of Nutrient Sensing in Yeasts.

FungiNet total, FungiNet C - Candida projects

Abstract (Expand)

UNLABELLED: Single-celled organisms have different strategies to sense and utilize nutrients in their ever-changing environments. The opportunistic fungal pathogen Candida albicans is a common member … of the human microbiota, especially that of the gastrointestinal (GI) tract. An important question concerns how C. albicans gained a competitive advantage over other microbes to become a successful commensal and opportunistic pathogen. Here, we report that C. albicans uses N-acetylglucosamine (GlcNAc), an abundant carbon source present in the GI tract, as a signal for nutrient availability. When placed in water, C. albicans cells normally enter the G0 phase and remain viable for weeks. However, they quickly lose viability when cultured in water containing only GlcNAc. We term this phenomenon GlcNAc-induced cell death (GICD). GlcNAc triggers the upregulation of ribosomal biogenesis genes, alterations of mitochondrial metabolism, and the accumulation of reactive oxygen species (ROS), followed by rapid cell death via both apoptotic and necrotic mechanisms. Multiple pathways, including the conserved cyclic AMP (cAMP) signaling and GlcNAc catabolic pathways, are involved in GICD. GlcNAc acts as a signaling molecule to regulate multiple cellular programs in a coordinated manner and therefore maximizes the efficiency of nutrient use. This adaptive behavior allows C. albicans' more efficient colonization of the gut. IMPORTANCE: The ability to rapidly and appropriately respond to nutrients in the environment is crucial to free-living microorganisms. To maximize the use of available nutrients, microorganisms often use a limiting nutritional component as a signal to coordinate multiple biological processes. The human fungal pathogen Candida albicans uses N-acetylglucosamine (GlcNAc) as a signal for the availability of external nutrient resources. GlcNAc induces rapid cell death in C. albicans due to the constitutive activation of oxidative metabolism and accumulation of reactive oxygen species (ROS), and multiple pathways are involved in its regulation. This study sheds light on the mechanisms of niche specialization of pathogenic fungi and raises the possibility that this cell death pathway could be an unexplored therapeutic target.

Authors: H. Du, G. Guan, X. Li, M. Gulati, L. Tao, C. Cao, A. D. Johnson, C. J. Nobile, G. Huang

Date Published: 10th Sep 2015

Publication Type: Not specified

PubMed ID: 26350972

Citation: MBio. 2015 Sep 8;6(5):e01376-15. doi: 10.1128/mBio.01376-15.

Created: 25th Sep 2017 at 10:53, Last updated: 17th Jan 2024 at 10:24

pH Regulates White-Opaque Switching and Sexual Mating in Candida albicans.

FungiNet C - Candida projects

Abstract (Expand)

As a successful commensal and pathogen of humans, Candida albicans encounters a wide range of environmental conditions. Among them, ambient pH, which changes frequently and affects many biological …

Authors: Y. Sun, C. Cao, W. Jia, L. Tao, G. Guan, G. Huang

Date Published: 6th Sep 2015

Publication Type: Not specified

PubMed ID: 26342021

Citation: Eukaryot Cell. 2015 Nov;14(11):1127-34. doi: 10.1128/EC.00123-15. Epub 2015 Sep 4.

Created: 15th Nov 2017 at 12:12, Last updated: 17th Jan 2024 at 10:24

View all 14 Publications