4.8 Article

Interactions Between Commensal Fungi and the C-Type Lectin Receptor Dectin-1 Influence Colitis

Journal

SCIENCE
Volume 336, Issue 6086, Pages 1314-1317

Publisher

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1221789

Keywords

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Funding

  1. National Institute of Allergy and Infectious Diseases, NIH [AI071116]
  2. Janis and William Wetsman Family Chair in Inflammatory Bowel Disease Research
  3. Crohn's and Colitis Foundation of America [3064]
  4. National Institute of Diabetes and Digestive and Kidney Diseases, NIH [P01-DK046763]
  5. UCLA Clinical and Translational Science Institute [UL1RR033176]
  6. Cedars-Sinai Medical Center Inflammatory Bowel and Immunobiology Research Institute
  7. Feintech Family Chair in IBD
  8. Cedars-Sinai Board of Governors' Chair in Medical Genetics
  9. Abe and Claire Levine Chair in Pediatric IBD
  10. Joshua L. and Lisa Z. Greer Chair in IBD Genetics
  11. 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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