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http://purl.uniprot.org/citations/21565393http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21565393http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21565393http://www.w3.org/2000/01/rdf-schema#comment"Inflammasomes are multiprotein complexes that function as sensors of endogenous or exogenous damage-associated molecular patterns. Here, we show that deficiency of NLRP6 in mouse colonic epithelial cells results in reduced IL-18 levels and altered fecal microbiota characterized by expanded representation of the bacterial phyla Bacteroidetes (Prevotellaceae) and TM7. NLRP6 inflammasome-deficient mice were characterized by spontaneous intestinal hyperplasia, inflammatory cell recruitment, and exacerbation of chemical colitis induced by exposure to dextran sodium sulfate (DSS). Cross-fostering and cohousing experiments revealed that the colitogenic activity of this microbiota is transferable to neonatal or adult wild-type mice, leading to exacerbation of DSS colitis via induction of the cytokine, CCL5. Antibiotic treatment and electron microscopy studies further supported the role of Prevotellaceae as a key representative of this microbiota-associated phenotype. Altogether, perturbations in this inflammasome pathway, including NLRP6, ASC, caspase-1, and IL-18, may constitute a predisposing or initiating event in some cases of human IBD."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2011.04.022"xsd:string
http://purl.uniprot.org/citations/21565393http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2011.04.022"xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Gordon J.I."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Gordon J.I."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Booth C.J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Booth C.J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Flavell R.A."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Flavell R.A."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Bertin J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Bertin J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Eisenbarth S.C."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Eisenbarth S.C."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Elinav E."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Elinav E."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Henao-Mejia J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Henao-Mejia J."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Strowig T."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Strowig T."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Thaiss C.A."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Thaiss C.A."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Kau A.L."xsd:string
http://purl.uniprot.org/citations/21565393http://purl.uniprot.org/core/author"Kau A.L."xsd:string