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Updated: Jan 6, 2026

An Ex vivo Assay to Study Candida albicans Hyphal Morphogenesis in the Gastrointestinal Tract
Published on: July 1, 2020
Candida albicans releases a peptide from the Rbt1 protein to promote its invasion into the gut epithelium
Hervé Bègue1,2, Amandine Ducreux1, Tracy Paradis1
1UMR PAM Univ Bourgogne Europe - Institut Agro Dijon - INRAE, Equipe Aliment, Fermentation, Interaction, Microbiote - AFIM, UFR Sciences de Santé, Dijon, France.
Abstract:
Candida albicans has been recently added to the WHO critical priority group of fungal pathogens based on its impact on global public health. C. albicans is a mucosal commensal yeast in humans that can cause severe gastrointestinal-borne disseminated candidiasis in immunocompromised patients. C. albicans interaction with enterocytes is thus a key step in the pathophysiology of disseminated candidiasis. Here, we show that, during the first steps of the infection process, C. albicans releases a peptide from the Repressed by Tup1 protein 1 (Rbt1), which disorganizes the cell‒cell adhesion junctions in Caco-2 intestinal epithelial cells by notably downregulating constitutive proteins of the tight junction complex (i.e. ZO-1). This is the first report to show that a peptide of a human pathogenic fungus promotes fungal invasion into the gut epithelium by disorganizing the protective epithelial barrier.
Insights
Candida albicans releases a peptide that disrupts intestinal cell adhesion, facilitating fungal invasion. This finding reveals a new mechanism for how this critical fungal pathogen breaches the gut barrier.
Area of Science:
- Medical Microbiology
- Infectious Diseases
- Cell Biology
Background:
- Candida albicans is a critical fungal pathogen prioritized by the WHO.
- It can cause disseminated candidiasis, particularly in immunocompromised individuals.
- Interaction with intestinal cells is crucial for gastrointestinal candidiasis.
Purpose of the Study:
- To investigate the molecular mechanisms of Candida albicans interaction with intestinal epithelial cells.
- To identify fungal factors involved in breaching the gut barrier.
Main Methods:
- Utilized Caco-2 intestinal epithelial cell models.
- Analyzed the effect of Candida albicans secreted peptides on cell-cell adhesion.
- Investigated the downregulation of tight junction proteins, including ZO-1.
Main Results:
- Candida albicans releases a peptide derived from the Repressed by Tup1 protein 1 (Rbt1).
- This Rbt1 peptide disorganizes cell-cell adhesion junctions in intestinal epithelial cells.
- The peptide downregulates key tight junction proteins like ZO-1, compromising the epithelial barrier.
Conclusions:
- A secreted peptide from Candida albicans actively disrupts the intestinal epithelial barrier.
- This mechanism facilitates fungal invasion into the host gut.
- This study uncovers a novel strategy employed by pathogenic fungi to initiate infection.
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