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Bull Acad Natl Med. 2012 Jan;196(1):139-49.

[The commensal-pathogen transition in invasive Candida albicans infection: molecular and cellular approaches].

[Article in French]

Author information

1
Laboratoire 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.

PMID:
23259341
[Indexed for MEDLINE]

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