Aarhus University Seal / Aarhus Universitets segl

Modulation of the fungal mycobiome is regulated by the chitin-binding receptor FIBCD1

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Jesper B. Moeller, Cornell University, University of Southern Denmark
  • ,
  • Irina Leonardi, Cornell University
  • ,
  • Anders Schlosser, University of Southern Denmark
  • ,
  • Anne Laure Flamar, Cornell University
  • ,
  • Nicholas J. Bessman, Cornell University
  • ,
  • Gregory Garbès Putzel, Cornell University
  • ,
  • Theresa Thomsen, University of Southern Denmark
  • ,
  • Mark Hammond, University of Southern Denmark
  • ,
  • Christine S. Jepsen, University of Southern Denmark
  • ,
  • Karsten Skjødt, University of Southern Denmark
  • ,
  • Ernst Martin Füchtbauer
  • Donna L. Farber, Columbia University in the City of New York
  • ,
  • Grith L. Sorensen, University of Southern Denmark
  • ,
  • Iliyan D. Iliev, Cornell University
  • ,
  • Uffe Holmskov, University of Southern Denmark
  • ,
  • David Artis, Cornell University

Host-microbiota interactions are critical in regulating mammalian health and disease. In addition to bacteria, parasites, and viruses, beneficial communities of fungi (the mycobiome) are important modulators of immune- and tissue-homeostasis. Chitin is a major component of the fungal cell wall, and fibrinogen C containing domain 1 (FIBCD1) is a chitin-binding protein; however, the role of this molecule in influencing host-mycobiome interactions in vivo has never been examined. Here, we identify direct binding of FIBCD1 to intestinal-derived fungi and demonstrate that epithelial-specific expression of FIBCD1 results in significantly reduced fungal colonization and amelioration of fungal-driven intestinal inflammation. Collectively, these results identify FIBCD1 as a previously unrecognized microbial pattern recognition receptor through which intestinal epithelial cells can recognize and control fungal colonization, limit fungal dysbiosis, and dampen intestinal inflammation.

Original languageEnglish
JournalThe Journal of Experimental Medicine
Pages (from-to)2689-2700
Number of pages12
Publication statusPublished - Dec 2019

Bibliographical note

© 2019 Moeller et al.

    Research areas

  • COLITIS, DOMAIN-CONTAINING 1, DYSBIOSIS, EXPRESSION, IMMUNITY, INFLAMMATORY RESPONSES, INNATE LYMPHOID-CELLS, PCR, SUSCEPTIBILITY, TRICHURIS-MURIS, Metagenomics, Humans, RNA, Ribosomal, 16S, Microbial Interactions, Disease Models, Animal, Gene Expression, DNA, Ribosomal Spacer, Mycobiome, Gastrointestinal Microbiome, Mice, Transgenic, Animals, Enteritis/etiology, Fungi/physiology, Intestinal Mucosa/metabolism, Protein Binding, Receptors, Cell Surface/metabolism, Mice, Chitin/metabolism

See relations at Aarhus University Citationformats

ID: 174162154