Modulation of the fungal mycobiome is regulated by the chitin-binding receptor FIBCD1
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...
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Published in | The Journal of experimental medicine Vol. 216; no. 12; pp. 2689 - 2700 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Rockefeller University Press
02.12.2019
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Abstract | 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. |
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AbstractList | 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. In the present study, Moeller et al. identify a previously unrecognized pathway through which intestinal epithelial cells expressing the novel chitin-binding receptor FIBCD1 can recognize and control intestinal fungal colonization, limit fungal dysbiosis, and dampen intestinal inflammation. 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. |
Author | Jepsen, Christine S Iliev, Iliyan D Hammond, Mark Flamar, Anne-Laure Bessman, Nicholas J Thomsen, Theresa Füchtbauer, Ernst-Martin Putzel, Gregory Garbès Leonardi, Irina Schlosser, Anders Moeller, Jesper B Skjødt, Karsten Holmskov, Uffe Artis, David Sorensen, Grith L Farber, Donna L |
AuthorAffiliation | 1 Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 3 Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark 4 Columbia Center for Translational Immunology, Department of Surgery and Department of Microbiology and Immunology, Columbia University, New York, NY 2 Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark |
AuthorAffiliation_xml | – name: 1 Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – name: 3 Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark – name: 2 Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – name: 4 Columbia Center for Translational Immunology, Department of Surgery and Department of Microbiology and Immunology, Columbia University, New York, NY |
Author_xml | – sequence: 1 givenname: Jesper B orcidid: 0000-0001-8786-8037 surname: Moeller fullname: Moeller, Jesper B email: jbmoeller@health.sdu.dk organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 2 givenname: Irina orcidid: 0000-0002-0369-7371 surname: Leonardi fullname: Leonardi, Irina organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – sequence: 3 givenname: Anders surname: Schlosser fullname: Schlosser, Anders organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 4 givenname: Anne-Laure surname: Flamar fullname: Flamar, Anne-Laure organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – sequence: 5 givenname: Nicholas J surname: Bessman fullname: Bessman, Nicholas J organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – sequence: 6 givenname: Gregory Garbès surname: Putzel fullname: Putzel, Gregory Garbès organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – sequence: 7 givenname: Theresa surname: Thomsen fullname: Thomsen, Theresa organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 8 givenname: Mark surname: Hammond fullname: Hammond, Mark organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 9 givenname: Christine S surname: Jepsen fullname: Jepsen, Christine S organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 10 givenname: Karsten surname: Skjødt fullname: Skjødt, Karsten organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 11 givenname: Ernst-Martin surname: Füchtbauer fullname: Füchtbauer, Ernst-Martin organization: Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark – sequence: 12 givenname: Donna L orcidid: 0000-0001-8236-9183 surname: Farber fullname: Farber, Donna L organization: Columbia Center for Translational Immunology, Department of Surgery and Department of Microbiology and Immunology, Columbia University, New York, NY – sequence: 13 givenname: Grith L surname: Sorensen fullname: Sorensen, Grith L organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 14 givenname: Iliyan D orcidid: 0000-0003-0884-9749 surname: Iliev fullname: Iliev, Iliyan D organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY – sequence: 15 givenname: Uffe surname: Holmskov fullname: Holmskov, Uffe organization: Department of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 16 givenname: David orcidid: 0000-0003-3608-1044 surname: Artis fullname: Artis, David email: dartis@med.cornell.edu organization: Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY dartis@med.cornell.edu |
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Snippet | Host-microbiota interactions are critical in regulating mammalian health and disease. In addition to bacteria, parasites, and viruses, beneficial communities... Host–microbiota interactions are critical in regulating mammalian health and disease. In addition to bacteria, parasites, and viruses, beneficial communities... In the present study, Moeller et al. identify a previously unrecognized pathway through which intestinal epithelial cells expressing the novel chitin-binding... |
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Title | Modulation of the fungal mycobiome is regulated by the chitin-binding receptor FIBCD1 |
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