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Interactions Between Commensal Fungi and the C-Type Lectin Receptor Dectin-1 Influence Colitis
Open accessAbstract
The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.
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“A recent study49 demonstrated that mice lacking Dectin1 had increased susceptibility to chemically induced colitis, due to their altered responses to indigenous fungi.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [49]
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“diet might also affect intestinal fungal communities, which have been associated with pathogenesis of inflammatory bowel diseases (IBD)49.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [49]
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“a polymorphism in the gene encoding Dectin1 (CLEC7A) was associated with a severe form of ulcerative colitis in humans49.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [49]
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Metadata
- Authors
- Iliev, I. D., Funari, V. A., Taylor, K. D., Nguyen, Q., Reyes, C. N., Strom, S. P., Brown, J., Becker, C. A., Fleshner, P. R., Dubinsky, M., Rotter, J. I., Wang, H. L., McGovern, D. P. B., Brown, G. D., & Underhill, D. M.
- Affiliations
- Cedars-Sinai Medical Center (US)
- University of California, Los Angeles (US)
- University of Aberdeen (GB)
- Corresponding author
- Underhill, David M.
- ORCID
- Venue
- Science
- Published
- 2012-06-08
- Volume
- 336
- Issue
- 6086
- Pages
- 1314-1317
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3432565
- OpenAlex
- W2036743290
- Cited by
- 1,073
- References
- 40
- Citations by year
- 2026: 36 · 2025: 64 · 2024: 54 · 2023: 74 · 2022: 75 · 2021: 111 · 2020: 79 · 2019: 98 · 2018: 70 · 2017: 84 · 2016: 67 · 2015: 67 · 2014: 84 · 2013: 88 · 2012: 22
- FWCI
- 33.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust (086558)
- Crohn's and Colitis Foundation
- National Institutes of Health (1ul1rr033176-01, UL1TR000124)
- National Institute of Allergy and Infectious Diseases (AI071116, R01AI071116)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK046763, R01DK093426)
- National Center for Research Resources (UL1-RR-033176)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- Dectin-1, commensal fungi, fungal communities, colitis, ulcerative colitis, innate immunity, intestinal immunity, chemically induced colitis, genetic polymorphism, inflammatory bowel disease
- MeSH terms
- Dectin-1, Animals, Antibodies, Fungal, Colitis, Ulcerative, Colon, Disease Susceptibility, Female, Fungi, Haplotypes, Humans, Immunity, Innate, Intestinal Mucosa, Intestines, Mice, Inbred C57BL, Colony Count, Microbial, Dextran Sulfate, Immunity, Mucosal, Polymorphism, Single Nucleotide, Lectins, C-Type, Candida tropicalis, Mice, Metagenome
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