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Published on: November 5, 2019
[The commensal-pathogen transition in invasive Candida albicans infection: molecular and cellular approaches]
1Laboratoire de parasitologie-mycologie, Plateau Technique de Biologie, CHU, 2, rue Angélique Ducoudray, BP 37013, 21070 Dijon cedex. alain.bonnin@u-bourgogne.fr
Abstract:
Invasive fungal infections (IFI) have become a major public health problem in industrialized countries, notably due to the increasing number of immunocompromized individuals. Endogenous candidiasis, arising from the patient's commensal flora, accounts for the majority of IFI. C albicans, generally originating from the colonized gastrointestinal tract, is the causative agent in about 50% of cases. Molecular and cellular investigations are helping to decipher the mechanisms underlying the commensal-pathogen transition. We have found that neutropenic patients are generally colonized by a single genotype, and that all C. albicans genotypes can cause invasive infection. By using epithelial cell-based models, we have shown that alpha 1, 2 and beta 1, 2 mannosides present in the outermost layer of the fungal cell wall mediate adherence to enterocytes. In addition, C. albicans uses different strategies for epithelial cell invasion, depending on the precise cell type with which it interacts.
Insights
Invasive fungal infections (IFI) are a growing concern, especially in immunocompromised individuals. Candida albicans, a common fungus, can transition from harmless commensal flora to a dangerous pathogen, causing IFI by adhering to and invading host cells.
Area of Science:
- Medical Mycology
- Infectious Diseases
- Molecular Biology
Background:
- Invasive fungal infections (IFI) pose a significant public health challenge, particularly in immunocompromised populations.
- Endogenous candidiasis, often caused by Candida albicans from the gut flora, is a major contributor to IFI.
- Understanding the transition of Candida albicans from commensal to pathogen is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the mechanisms underlying the commensal-pathogen transition of Candida albicans.
- To identify fungal cell wall components involved in host cell adherence and invasion.
- To explore genotype-specific aspects of Candida albicans colonization and infection.
Main Methods:
- Utilized epithelial cell-based models to study fungal-host interactions.
- Employed molecular and cellular investigation techniques.
- Analyzed Candida albicans colonization patterns in neutropenic patients.
Main Results:
- Neutropenic patients are typically colonized by a single Candida albicans genotype, and all genotypes are capable of causing invasive infections.
- Alpha 1,2 and beta 1,2 mannosides in the fungal cell wall mediate adherence to enterocytes.
- Candida albicans employs distinct invasion strategies depending on the specific epithelial cell type.
Conclusions:
- Candida albicans adherence to the gut epithelium is mediated by specific mannosides.
- The fungus exhibits adaptable invasion mechanisms targeting different host cell types.
- All genotypes of Candida albicans possess the potential to cause invasive disease in susceptible individuals.
