Conclusion
The rapid emergence of IBD worldwide is likely to be the consequence of environmental and genetic influence associated with alterations of the gut microbiota resulting in a dysregulated immune response in the host. Recent fungal sequencing analysis revealed an expansion of the fungi Candida and Malassezia in the stool and mucosa of IBD patients. Genetic deficiency at the CARD9 loci was also found to be associated with disease severity in IBD. In animal studies, supplementation of C albicans, C tropicalis (particularly in CARD9 deficient setting) and S cerevisiae exacerbates colitis progression whereby one possible mechanism is via increased intestinal permeability and modulated host purine metabolism. In addition to genetic factors, fungal alterations are triggered by environmental factors including diet. Modulation of the fungal microbiota can be considered as a therapeutic opportunity for IBD, as certain strains including S boulardii, S cerevisiae CNCM I-3856 strain and S fibuligera have shown therapeutic effects in human and murine IBD models. Future research should focus on enhancing our understanding on how the fungal microbiota interacts with other components of the gut microbiota and the mechanisms of these interactions, in association with the pathogenesis and development of IBD.
Authorship
Guarantor of the article
Siew Ng.
Funding information
None.
Aliment Pharmacol Ther. 2019;50(11):1159-1171. © 2019 Blackwell Publishing
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