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Updated: Feb 6, 2026

Visualization of Candida albicans in the Murine Gastrointestinal Tract Using Fluorescent In Situ Hybridization
Published on: November 5, 2019
Intestinal epithelial cells and T cells differentially recognize and respond to Candida albicans yeast and hypha
Anja Schirbel1, Dror S Shouval2,3, Betty Hebecker4,5
1Department of Medicine, Division of Gastroenterology and Hepatology, Charité Campus Mitte, Universitätsmedizin Berlin, Germany.
Abstract:
Inflammatory bowel diseases (IBD) are a multifactorial disorder. Our understanding of the role of bacteria in the pathogenesis of IBD has increased substantially; however, only scarce data exist regarding the role of commensal fungi in maintaining intestinal homeostasis and triggering IBD. Candida albicans (C. albicans) is a member of the intestinal mycobiome and proposed to contribute to IBD pathogenesis. We aimed to investigate the influence of the two morphologies of C. albicans, yeast and hypha, on epithelial cells and T cells from IBD patients versus healthy controls. We found that C. albicans was recognized by both epithelial cells lines and T cells. In the intestinal epithelial cell line, Caco-2, response to hypha was different than to yeast cells, and this was mimicked by synthetic β-glucans and Pam3CSK4. Unstimulated T cells exhibited increased activation and pro-inflammatory cytokine secretion upon exposure, while there was no effect on apoptosis or proliferation. In contrast, C. albicans-challenged CD3-stimulated T-cells exhibited decreased activation, cytokine secretion, apoptosis, and proliferation, suggesting reciprocal responsiveness to C. albicans. Glycans alone did not mimic abovementioned influences on T cells, suggesting alternative modes of recognition. In conclusion, we provide evidence for glycan dependent and independent recognition of C. albicans by epithelial cells and T cells.
Insights
The study investigated how Candida albicans (fungus) affects intestinal cells and immune cells in inflammatory bowel diseases (IBD). Findings show C. albicans influences cell responses differently depending on its form, impacting IBD pathogenesis.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Inflammatory bowel diseases (IBD) are complex disorders with increasing focus on microbial roles.
- While bacterial involvement is well-studied, the contribution of intestinal fungi, like Candida albicans, to IBD pathogenesis remains less understood.
- Candida albicans is a common gut fungus that may play a role in maintaining intestinal homeostasis or triggering IBD.
Purpose of the Study:
- To investigate the differential effects of Candida albicans yeast and hyphal forms on intestinal epithelial cells and T cells.
- To compare responses in cells from patients with IBD versus healthy individuals.
- To elucidate the mechanisms of C. albicans recognition by host cells.
Main Methods:
- Utilized Caco-2 intestinal epithelial cell lines and primary T cells from IBD patients and healthy controls.
- Exposed cells to different morphologies of C. albicans (yeast and hypha).
- Assessed cellular responses including activation, cytokine secretion, apoptosis, and proliferation, using synthetic agonists like β-glucans and Pam3CSK4 for comparison.
Main Results:
- C. albicans elicited distinct responses from Caco-2 cells depending on its morphology (yeast vs. hypha), partly mimicked by synthetic agonists.
- Unstimulated T cells showed increased activation and pro-inflammatory cytokine secretion upon C. albicans exposure.
- T cells stimulated with CD3 and C. albicans exhibited reduced activation, cytokine secretion, apoptosis, and proliferation, indicating complex reciprocal interactions.
- Glycans alone did not fully replicate the observed effects on T cells, suggesting non-glycan-mediated recognition pathways.
Conclusions:
- Candida albicans recognition by intestinal epithelial cells and T cells is multifaceted, involving both glycan-dependent and independent mechanisms.
- The distinct morphologies of C. albicans influence host cell responses, potentially contributing to the inflammatory processes in IBD.
- Further research is needed to fully understand the role of the intestinal mycobiome in IBD pathogenesis and host-microbe interactions.
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