Nature Communications (Sep 2018)
NLRP1 restricts butyrate producing commensals to exacerbate inflammatory bowel disease
- Hazel Tye,
- Chien-Hsiung Yu,
- Lisa A. Simms,
- Marcel R. de Zoete,
- Man Lyang Kim,
- Martha Zakrzewski,
- Jocelyn S. Penington,
- Cassandra R. Harapas,
- Fernando Souza-Fonseca-Guimaraes,
- Leesa F. Wockner,
- Adele Preaudet,
- Lisa A. Mielke,
- Stephen A. Wilcox,
- Yasunori Ogura,
- Sinead C. Corr,
- Komal Kanojia,
- Konstantinos A. Kouremenos,
- David P. De Souza,
- Malcolm J. McConville,
- Richard A. Flavell,
- Motti Gerlic,
- Benjamin T. Kile,
- Anthony T. Papenfuss,
- Tracy L. Putoczki,
- Graham L. Radford-Smith,
- Seth L. Masters
Affiliations
- Hazel Tye
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Chien-Hsiung Yu
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Lisa A. Simms
- Gut Health, QIMR Berghofer Medical Research Institute
- Marcel R. de Zoete
- Department of Immunobiology, Yale University School of Medicine
- Man Lyang Kim
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Martha Zakrzewski
- Medical Genomics, QIMR Berghofer Medical Research Institute
- Jocelyn S. Penington
- Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research
- Cassandra R. Harapas
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Fernando Souza-Fonseca-Guimaraes
- Department of Medical Biology, University of Melbourne
- Leesa F. Wockner
- Statistics Division, QIMR Berghofer Medical Research Institute
- Adele Preaudet
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Lisa A. Mielke
- Department of Medical Biology, University of Melbourne
- Stephen A. Wilcox
- Department of Medical Biology, University of Melbourne
- Yasunori Ogura
- Department of Food Science and Nutrition, Nara Women’s University
- Sinead C. Corr
- Department of Microbiology, The Moyne Institute of Preventative Medicine, School of Genetics and Microbiology, Trinity College Dublin
- Komal Kanojia
- Metabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne
- Konstantinos A. Kouremenos
- Metabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne
- David P. De Souza
- Metabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne
- Malcolm J. McConville
- Metabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne
- Richard A. Flavell
- Department of Immunobiology, Yale University School of Medicine
- Motti Gerlic
- Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University
- Benjamin T. Kile
- Department of Medical Biology, University of Melbourne
- Anthony T. Papenfuss
- Department of Medical Biology, University of Melbourne
- Tracy L. Putoczki
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- Graham L. Radford-Smith
- Gut Health, QIMR Berghofer Medical Research Institute
- Seth L. Masters
- Inflammation Division, The Walter and Eliza Hall Institute of Medical Research
- DOI
- https://doi.org/10.1038/s41467-018-06125-0
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 11
Abstract
The inflammasome is normally activated by pathogens to induce tissue inflammation. Here the authors show that, in mouse experimental colitis models, Nlrp1 inflammasome sensor activates IL-18 to reduce beneficial colonic Clostridiales species, thereby decreasing microbial butyrate and its protective effects on colitis.
