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

TitleInteractions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis.
Publication TypeJournal Article
Year of Publication2012
AuthorsIliev ID, Funari VA, Taylor KD, Nguyen Q, Reyes CN, Strom SP, Brown J, Becker CA, Fleshner PR, Dubinsky M, Rotter JI, Wang HL, McGovern DPB, Brown GD, Underhill DM
JournalScience
Volume336
Issue6086
Pagination1314-7
Date Published2012 Jun 8
ISSN1095-9203
KeywordsAnimals, 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
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.

DOI10.1126/science.1221789
Alternate JournalScience
PubMed ID22674328
PubMed Central IDPMC3432565
Grant List086558 / / Wellcome Trust / United Kingdom
AI071116 / AI / NIAID NIH HHS / United States
P01-DK046763 / DK / NIDDK NIH HHS / United States
R01 DK093426 / DK / NIDDK NIH HHS / United States
UL1 RR033176 / RR / NCRR NIH HHS / United States
UL1 TR000124 / TR / NCATS NIH HHS / United States
UL1RR033176 / RR / NCRR NIH HHS / United States
/ / Wellcome Trust / United Kingdom