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Microbial Ecology in States of Health and Disease Workshop Summary (2014) / Chapter Skim
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A18 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, and David M. Underhill
Pages 435-444

The Chapter Skim interface presents what we've algorithmically identified as the most significant single chunk of text within every page in the chapter.
Select key terms on the right to highlight them within pages of the chapter.


From page 435...
... . 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.
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From page 436...
... that is strongly linked to a severe form of ulcerative colitis. Together our findings reveal a novel eukaryotic fungal community in the gut (the "­ ycobiome")
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From page 437...
... ITS1-2 rDNA level was analyzed by quantitative polymerase chain reaction and normalized to β-actin DNA.
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From page 438...
... We know very little about what commensal fungi populate the murine gut or how they contribute to colitis in Dectin-1 deficiency. To define the mouse intestinal fungal microbiome, we isolated DNA from murine feces, amplified the internal transcribed spacer region (ITS1-2)
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From page 439...
... One study has reported increased fungal burden in intestines of Crohn's disease patients (Ott et al., 2008) , and another has shown increased colonization with exogenously added C
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From page 440...
... The taxonomic distribution of the most abundant fungal genera is shown (large pie chart) , and the species breakdowns for major groups are provided (small pie charts)
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From page 441...
... . The data suggest that an inability of Clec7a−/− mice to mount effective immune responses to specific intestinal fungi creates conditions that promote inflammation.
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From page 442...
... Unlike susceptibility genes that predispose to disease, severity gene variants aggravate disease that is initially established through other mechanisms. The CLEC7A risk haplotype we report here fits the latter situation and agrees with our observation that Clec7a−/− mice do not develop spontaneous colitis.
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From page 443...
... from the Crohn's and Colitis Foundation of America. Further support came from National Institute of Diabetes and Digestive and Kidney Diseases, NIH, grant P01-DK046763; UCLA Clinical and Translational Science Institute grant UL1RR033176; Cedars-Sinai Medical Center Inflammatory Bowel and Immunobiology Research Institute Funds; The ­ eintech Family Chair in IBD (S.
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From page 444...
... Accurate taxonomy assignments from 16S rRNA s ­ equences produced by highly parallel pyrosequencers. Nucleic Acids Res.
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Key Terms

  • ulcerative colitis
  • microbial ecology
  • commensal fungi
  • dendritic cells
  • fungal genera

  • strongly associated
  • immune responses
  • histology score
  • bowel disease
  • medically refractory

  • mice supplemented
  • immunobiology research
  • dss colitis
  • fungal species
  • error bars

  • cytokine production
  • medical genetics
  • family chair
  • findings suggest
  • similar results

  • david geffen
  • fungal community
  • colonic tissue
  • raw data
  • fungal burden

  • dss treatment
  • disease severity
  • independent experiments
  • commensal bacteria
  • fungal infections


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