How Gut Bacterial Dysbiosis Can Promote Candida albicans Overgrowth during Colonic Inflammation

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, beta-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 beta-glucans and chitin, on the modification of the gut microbiota, as well as how these glycans modulate the immuno-inflammatory response of the host.

Automated summary

Candida albicans, an opportunistic yeast, can cause invasive fungal infections when it overgrows in the gut due to factors such as immunosuppression, antibiotic treatment, and changes in the gut microbiota and digestive mucosa. The cell wall components of C. albicans, including mannoproteins, beta-glucans, and chitin, play a role in host cell activities and circulate in the blood during fungal infections. This review discusses the involvement of various receptors, such as mannose-binding lectin (MBL) and toll-like receptors (TLRs), in the immune defense against C. albicans in the intestine. It also highlights the dysbiosis of the gut microbiota during colonic inflammation and the effects of fungal glycan fractions, specifically beta-glucans and chitin, on the gut microbiota and host immune response.