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  • Review Article
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Mycobiota in gastrointestinal diseases

Key Points

  • The mycobiome (the resident fungal community and their genome), is a key component of the human microbiome

  • Within a microbiome, there are interactions between and within species or genera among fungi and bacteria

  • Alterations within the mycobiota are associated with different diseases

  • The mycobiota might directly or indirectly interact with the host immune system

  • Interactions between the mycobiota and host immune system can lead to exacerbation of gastrointestinal diseases such as IBD

Abstract

New insights gained through the use of state-of-the-art technologies, including next-generation sequencing, are starting to reveal that the association between the gastrointestinal tract and the resident mycobiota (fungal community) is complex and multifaceted, in which fungi are active participants influencing health and disease. Characterizing the human mycobiome (the fungi and their genome) in healthy individuals showed that the gastrointestinal tract contains 66 fungal genera and 184 fungal species, with Candida as the dominant fungal genera. Although fungi have been associated with a number of gastrointestinal diseases, characterization of the mycobiome has mainly been focused on patients with IBD and graft-versus-host disease. In this Review, we summarize the findings from studies investigating the relationship between the gut mycobiota and gastrointestinal diseases, which indicate that fungi contribute to the aggravation of the inflammatory response, leading to increased disease severity. A model explaining the mechanisms underlying the role of the mycobiota in gastrointestinal diseases is also presented. Our understanding of the contribution of the mycobiota to health and disease is still in its infancy and leaves a number of questions to be addressed. Answering these questions might lead to novel approaches to prevent and/or manage acute as well as chronic gastrointestinal disease.

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Figure 1: Normal and abnormal interactions between fungi and the host immune system in gastrointestinal tissue.

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Acknowledgements

Funding support is acknowledged from the NIH/NIDCR [RO1DE17846, R01DE024228 and the Oral HIV AIDS Research Alliance (BRS-ACURE-S-11-000049-110229 and AI-U01-68636) to M.A.G. Support from NIH/NEI and NIH/NIAID (R21EY021303 and R21AI074077), pilot funding from the Infectious Diseases Drug Development Center (IDDDC, Case), the National Eczema Association (Research Grant) and the National Psoriasis Foundation (Discovery Award) to P.K.M. Support from the CWRU/UH Center for AIDS Research (CFAR, NIH grant number P30 AI036219) and funding from the European Community's Seventh Framework Programme (FP7-2007-2013) under HEALTH-F2-2010-260338-ALLFUN and by the Programme Hospitalier de Recherche Clinique du Ministère des Affaires Sociales, de la Santé et de la Ville PHRC 1918, 2011 Candigène, France, to B.S.

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M.A.G., P.K.M. and B.S. contributed to researching data, substantial discussion of content, writing, reviewing and editing the manuscript. G.H., J.-F.C. and D.P. substantially contributed to discussion of content, reviewing and editing the manuscript.

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Correspondence to Mahmoud A. Ghannoum.

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Competing interests

J.-F.C. has served as consultant, advisory board member or speaker for Abbvie, ABScience, Amgen, Bristol–Meyers Squibb, Celltrion, Danone, Ferring, Genentech, Giuliani SPA, Given Imaging, Janssen, Immune Pharmaceuticals, Merck, Millenium Pharmaceuticals, Nutrition Science Partners, Pfizer, Prometheus Laboratories, Protagonist Therapeutics, Receptos, Sanofi, Schering Plough, Second Genome, Takeda, Teva Pharmaceuticals, UCB Pharma, Vertex and Dr August Wolff. P.K.M., B.S., G.H., D.P. and M.A.G. declare no competing interests.

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Mukherjee, P., Sendid, B., Hoarau, G. et al. Mycobiota in gastrointestinal diseases. Nat Rev Gastroenterol Hepatol 12, 77–87 (2015). https://doi.org/10.1038/nrgastro.2014.188

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