Evidence map›Paper›PMID 30214011›Full record

ArticleNature communications2018

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 and 16 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 112 citations in OpenAlex.

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  17. Heliyon · 2023
    Article
  18. Gut microbiota and neonatal acute kidney injury biomarkers.Pediatric nephrology (Berlin, Germany) · 2023
    Review
  19. Nutrients · 2023
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors at 9 institutions in 6 countries.

Hazel TyeInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Chien-Hsiung YuInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Lisa A SimmsGut Health, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australia.
Marcel R de ZoeteDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, 06519, USA.
Man Lyang KimInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Martha ZakrzewskiMedical Genomics, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australia.
Jocelyn S PeningtonBioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.ORCID http://orcid.org/0000-0003-1561-0074
Cassandra R HarapasInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Fernando Souza-Fonseca-GuimaraesDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Leesa F WocknerStatistics Division, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australia.ORCID http://orcid.org/0000-0002-8921-9265
Adele PreaudetInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Lisa A MielkeDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Stephen A WilcoxDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Yasunori OguraDepartment of Food Science and Nutrition, Nara Women's University, Nara, 6308506, Japan.
Sinead C CorrDepartment of Microbiology, The Moyne Institute of Preventative Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin 2, Ireland.
Komal KanojiaMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, VIC, 3010, Australia.
Konstantinos A KouremenosMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, VIC, 3010, Australia.
David P De SouzaMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, VIC, 3010, Australia.
Malcolm J McConvilleMetabolomics Australia, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Parkville, VIC, 3010, Australia.
Richard A FlavellDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, 06519, USA.
Motti GerlicDepartment of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel.ORCID http://orcid.org/0000-0001-9518-1833
Benjamin T KileDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Anthony T PapenfussDepartment of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.ORCID http://orcid.org/0000-0002-1102-8506
Tracy L PutoczkiInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Graham L Radford-SmithGut Health, QIMR Berghofer Medical Research Institute, Brisbane, 4029, QLD, Australia.ORCID http://orcid.org/0000-0002-2047-6239
Seth L MastersInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia. masters@wehi.edu.au.ORCID http://orcid.org/0000-0003-4763-576X
The University of Melbourne · AUQIMR Berghofer Medical Research Institute · AUHoward Hughes Medical Institute · USNara Women's University · JPTel Aviv University · ILThe University of Queensland · AUTrinity College Dublin · IEUtrecht University · NLWalter and Eliza Hall Institute of Medical Research · AU

Funding

Wellcome Trust 208694/Z/17/Z
6 · The paper itself

Abstract

Anti-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.

Indexed as

EubacterialesAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsButyratesColitisColonFemaleGastrointestinal MicrobiomeGene DeletionHumansInflammasomesInflammatory Bowel DiseasesInterferon-gammaInterleukin-18Intestinal MucosaAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsButyratesInflammasomesInterferon-gammaInterleukin-18NALP1 protein, mouseNLRP1 protein, humanNLR ProteinsVancomycin

Identifiers

PMID30214011
PMCPMC6137172
OpenAlexW2890485373

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.