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How Gut Bacterial Dysbiosis Can Promote Candida albicans Overgrowth during Colonic Inflammation
1UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale U1285, Université Lille, F-59000 Lille, France.
Abstract:
Candida albicans is a commensal opportunistic yeast, which is capable of colonising many segments of the human digestive tract. Excessive C. albicans overgrowth in the gut is associated with multiple risk factors such as immunosuppression, antibiotic treatment associated with changes to the gut microbiota and digestive mucosa that support C. albicans translocation across the digestive intestinal barrier and haematogenous dissemination, leading to invasive fungal infections. The C. albicans cell wall contains mannoproteins, β-glucans, and chitin, which are known to trigger a wide range of host cell activities and to circulate in the blood during fungal infection. This review describes the role of C. albicans in colonic inflammation and how various receptors are involved in the immune defence against C. albicans with a special focus on the role of mannose-binding lectin (MBL) and TLRs in intestinal homeostasis and C. albicans sensing. This review highlights gut microbiota dysbiosis during colonic inflammation in a dextran sulphate sodium (DSS)-induced colitis murine model and the effect of fungal glycan fractions, in particular β-glucans and chitin, on the modification of the gut microbiota, as well as how these glycans modulate the immuno-inflammatory response of the host.
Insights
Candida albicans overgrowth can cause invasive fungal infections. This review explores how gut microbiota and fungal components like beta-glucans and chitin influence immune responses in colonic inflammation.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Candida albicans is a common gut yeast that can overgrow due to factors like immunosuppression and antibiotics.
- C. albicans translocation across the gut barrier can lead to invasive fungal infections.
- The yeast cell wall components (mannoproteins, beta-glucans, chitin) activate host immune responses.
Purpose of the Study:
- To review the role of C. albicans in colonic inflammation.
- To highlight the involvement of immune receptors, specifically mannose-binding lectin (MBL) and Toll-like receptors (TLRs), in C. albicans sensing and intestinal homeostasis.
- To examine gut microbiota dysbiosis and the impact of fungal glycans on host immune response during colitis.
Main Methods:
- Literature review focusing on C. albicans, colonic inflammation, and immune responses.
- Discussion of host immune receptors (MBL, TLRs) involved in sensing C. albicans.
- Analysis of a dextran sulphate sodium (DSS)-induced colitis murine model to study gut microbiota and fungal glycan effects.
Main Results:
- Gut microbiota dysbiosis is observed during colonic inflammation.
- Fungal glycan fractions (beta-glucans, chitin) can modify the gut microbiota composition.
- These glycans modulate the host's immuno-inflammatory response.
Conclusions:
- C. albicans plays a significant role in colonic inflammation.
- Immune receptors like MBL and TLRs are crucial for intestinal homeostasis and C. albicans detection.
- Fungal glycans influence gut microbiota and host immune responses, offering potential therapeutic targets.
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