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.

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Publisher Full Text

Authors

Iliev ID, Funari VA, Taylor KD, Nguyen Q, Reyes CN, Strom SP, Brown J, Becker CA, Fleshner PR, Dubinsky M, Rotter JI, Wang HL, McGovern DP, Brown GD, Underhill DM

Institution

Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

Source

Science (New York, N.Y.) 336:6086 2012 Jun 8 pg 1314-7

MeSH

Animals
Antibodies, Fungal
Candida tropicalis
Colitis, Ulcerative
Colon
Colony Count, Microbial
Dextran Sulfate
Disease Susceptibility
Female
Fungi
Haplotypes
Humans
Immunity, Innate
Immunity, Mucosal
Intestinal Mucosa
Intestines
Lectins, C-Type
Metagenome
Mice
Mice, Inbred C57BL
Polymorphism, Single Nucleotide

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22674328