Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis

Iliyan D Iliev, Vincent A Funari, Kent D Taylor, Quoclinh Nguyen, Christopher N Reyes, Samuel P Strom, Jordan Brown, Courtney A Becker, Phillip R Fleshner, Marla Dubinsky, Jerome I Rotter, Hanlin L Wang, Dermot P B McGovern, Gordon D Brown, David M Underhill

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522 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)1314-1317
Number of pages4
JournalScience
Volume336
Issue number6086
Early online date6 Jun 2012
DOIs
Publication statusPublished - 8 Jun 2012

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    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. (2012). Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis. Science, 336(6086), 1314-1317. https://doi.org/10.1126/science.1221789