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Fungal microbiota dysbiosis in IBD
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Published: 6 years ago

Fungal microbiota dysbiosis in IBD


Crohn's disease (CD) and UC, the two primary types of IBD, are lifelong conditions that usually affect young subjects and substantially alter their quality of life. The exact pathogenesis of IBD remains unknown; however, studies over the last decade have demonstrated that IBD involves an altered immune response towards gut microbiota in genetically predisposed subjects and under the influence of environmental factors.

The bacterial microbiota in IBD has been thoroughly investigated, and several groups worldwide observed a bacterial dysbiosis (an imbalance in composition) that is characterised by a reduced biodiversity, a decrease in some bacteria belonging to the Firmicutes phylum (such as Faecalibacterium prausnitzii) and an increase in bacteria belonging to the Proteobacteria phylum such as Escherichia coli.1–5 However, other microorganism types colonising the human gut have not been thoroughly investigated. With the exception of a recent study highlighting the possible role of the enteric virome in IBD,6 the data are scarce, particularly regarding fungal microbiota.

Fungi have long been suspected in IBD pathogenesis. Many years ago, antibodies directed against Saccharomyces cerevisiae mannan (Anti Saccharomyces cerevisiae antibody (ASCA)) were shown to be associated with CD. Moreover, several IBD-associated genes, such as Card9, are involved in immune responses to fungi.7 In mice, gut inflammation promotes fungi proliferation;8 conversely, some fungi can modulate susceptibility to inflammation in a negative (Candida albicans) or positive (Saccharomyces boulardii) manner.8–11 Finally, mice lacking major genes involved in fungi sensing, such as Dectin-1 or Card9, have an increased fungal microbiota load and are more susceptible to colitis.12 ,13 These data suggest a link between fungal microbiota and IBD pathogenesis.

Here, we characterised the fungal microbiota in both healthy subjects (HS) and patients with well-phenotyped IBD using high-throughput sequencing technology. In the corresponding patients, we also determined the bacterial microbiota composition and the sequence of 22 single-nucleotide polymorphisms (SNPs) in genes known to be involved in fungal susceptibility. We observed a clear fungal dysbiosis in patients with IBD. Moreover, a correlation analysis suggested altered inter-kingdom relations in IBD. Finally, while somewhat lacking in power, our genotype–fungal microbiota analysis suggested that genes may be a driving factor of the fungal microbiota dysbiosis in IBD.

Overall, the data presented in this study represent the most comprehensive analysis of fungal microbiota in patients with IBD to date and provide a rationale to support the role of fungal microbiota in IBD pathogenesis. These data thus pave the way for intervention studies targeting fungal microbiota.

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