Journal
SCIENCE
Volume 336, Issue 6086, Pages 1314-1317Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1221789
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Funding
- National Institute of Allergy and Infectious Diseases, NIH [AI071116]
- Janis and William Wetsman Family Chair in Inflammatory Bowel Disease Research
- Crohn's and Colitis Foundation of America [3064]
- National Institute of Diabetes and Digestive and Kidney Diseases, NIH [P01-DK046763]
- UCLA Clinical and Translational Science Institute [UL1RR033176]
- Cedars-Sinai Medical Center Inflammatory Bowel and Immunobiology Research Institute
- Feintech Family Chair in IBD
- Cedars-Sinai Board of Governors' Chair in Medical Genetics
- Abe and Claire Levine Chair in Pediatric IBD
- Joshua L. and Lisa Z. Greer Chair in IBD Genetics
- Wellcome Trust
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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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