Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/19589
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dc.contributor.authorTye, Hazel-
dc.contributor.authorYu, Chien-Hsiung-
dc.contributor.authorSimms, Lisa A-
dc.contributor.authorde Zoete, Marcel R-
dc.contributor.authorKim, Man Lyang-
dc.contributor.authorZakrzewski, Martha-
dc.contributor.authorPenington, Jocelyn S-
dc.contributor.authorHarapas, Cassandra R-
dc.contributor.authorSouza-Fonseca-Guimaraes, Fernando-
dc.contributor.authorWockner, Leesa F-
dc.contributor.authorPreaudet, Adele-
dc.contributor.authorMielke, Lisa A-
dc.contributor.authorWilcox, Stephen A-
dc.contributor.authorOgura, Yasunori-
dc.contributor.authorCorr, Sinead C-
dc.contributor.authorKanojia, Komal-
dc.contributor.authorKouremenos, Konstantinos A-
dc.contributor.authorDe Souza, David P-
dc.contributor.authorMcConville, Malcolm J-
dc.contributor.authorFlavell, Richard A-
dc.contributor.authorGerlic, Motti-
dc.contributor.authorKile, Benjamin T-
dc.contributor.authorPapenfuss, Anthony T-
dc.contributor.authorPutoczki, Tracy L-
dc.contributor.authorRadford-Smith, Graham L-
dc.contributor.authorMasters, Seth L-
dc.date2018-09-13-
dc.date.accessioned2018-10-11T02:51:44Z-
dc.date.available2018-10-11T02:51:44Z-
dc.date.issued2018-09-13-
dc.identifier.citationNature Communications 2018; 9(1): 3728-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/19589-
dc.description.abstractAnti-microbial signaling pathways are normally triggered by innate immune receptors when detecting pathogenic microbes to provide protective immunity. Here we show that the inflammasome sensor Nlrp1 aggravates DSS-induced experimental mouse colitis by limiting beneficial, butyrate-producing Clostridiales in the gut. The colitis-protective effects of Nlrp1 deficiency are thus reversed by vancomycin treatment, but recapitulated with butyrate supplementation in wild-type mice. Moreover, an activating mutation in Nlrp1a increases IL-18 and IFNγ production, and decreases colonic butyrate to exacerbate colitis. We also show that, in patients with ulcerative colitis, increased NLRP1 in inflamed regions of the colon is associated with increased IFN-γ. In this context, NLRP1, IL-18 or IFN-γ expression negatively correlates with the abundance of Clostridiales in human rectal mucosal biopsies. Our data identify the NLRP1 inflammasome to be a key negative regulator of protective, butyrate-producing commensals, which therefore promotes inflammatory bowel disease.-
dc.language.isoeng-
dc.titleNLRP1 restricts butyrate producing commensals to exacerbate inflammatory bowel disease.-
dc.typeJournal Article-
dc.identifier.journaltitleNature Communications-
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australiaen
dc.identifier.affiliationDepartment of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israelen
dc.identifier.affiliationACRF Chemical Biology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australiaen
dc.identifier.affiliationDepartment of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, 3800, Victoria, Australiaen
dc.identifier.affiliationSir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, 3010, Australiaen
dc.identifier.affiliationBioinformatics and Cancer Genomics Lab, Peter MacCallum Cancer Centre, Melbourne, VIC, 3002, Australiaen
dc.identifier.affiliationDepartment of Gastroenterology, Royal Brisbane and Women's Hospital, Brisbane, 4029, QLD, Australiaen
dc.identifier.affiliationUniversity of Queensland School of Medicine, Brisbane, 4029, QLD, Australiaen
dc.identifier.affiliationInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australiaen
dc.identifier.affiliationDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australiaen
dc.identifier.affiliationGut Health, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australiaen
dc.identifier.affiliationDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, 06519, USAen
dc.identifier.affiliationDepartment of Infectious Diseases and Immunology, Utrecht University, Utrecht, 3584 CL, The Netherlandsen
dc.identifier.affiliationMedical Genomics, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australiaen
dc.identifier.affiliationBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australiaen
dc.identifier.affiliationMolecular Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australiaen
dc.identifier.affiliationStatistics Division, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australiaen
dc.identifier.affiliationSystems Biology and Personalized Medicine Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australiaen
dc.identifier.affiliationDepartment of Food Science and Nutrition, Nara Women's University, Nara, 6308506, Japanen
dc.identifier.affiliationDepartment of Microbiology, The Moyne Institute of Preventative Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin 2, Irelanden
dc.identifier.affiliationMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, VIC, 3010, Australiaen
dc.identifier.affiliationDepartment of Biochemistry and Molecular Biology, Parkville, VIC, 3010, Australiaen
dc.identifier.affiliationHoward Hughes Medical Institute, Yale University, New Haven, CT, 06510, USAen
dc.identifier.doi10.1038/s41467-018-06125-0-
dc.identifier.orcid0000-0003-1561-0074-
dc.identifier.orcid0000-0002-8921-9265-
dc.identifier.orcid0000-0001-9518-1833-
dc.identifier.orcid0000-0002-1102-8506-
dc.identifier.orcid0000-0002-2047-6239-
dc.identifier.orcid0000-0003-4763-576X-
dc.identifier.pubmedid30214011-
dc.type.austinJournal Article-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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