ArticleNature communications2018
NLRP1 restricts butyrate producing commensals to exacerbate inflammatory bowel disease.
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.
What it found
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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.
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.
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Who cites it
57 citing papers in PubMed, 112 citations in OpenAlex.
- Inflammasomes in digestive diseases: mechanisms and therapeutic potential.Molecular biology reports · 2026Review
- NLRPs and tumor: research progress from molecular mechanisms to clinical applications.Oncogene · 2026Review
- Gastrointestinal microbiota and inflammasomes interplay in health and disease: a gut feeling.Gut · 2025Review
- Research progress concerning the involvement of the intestinal microbiota in the occurrence and development of inflammatory bowel disease.World journal of gastroenterology · 2025Review
- Goat-derived Lactobacillus amylovorus improved floppy kid syndrome via regulating gut microflora.BMC veterinary research · 2025Article
- Microbiota in inflammatory bowel disease: mechanisms of disease and therapeutic opportunities.Nature reviews. Microbiology · 2025Review
- Integrated 16S rDNA-Seq and metabolomics reveal seasonal dynamics of gut microbial-SCFA-immune crosstalk in diarrheic calves.Frontiers in veterinary science · 2025Article
- Gut microbiota and their metabolites ameliorate acute and chronic colitis in mice via modulating Th17/Treg balance.Frontiers in microbiology · 2025Article
- Fecal microbiota and metabolites in the pathogenesis and precision medicine for inflammatory bowel disease.Precision clinical medicine · 2024Review
- The interaction of inflammasomes and gut microbiota: novel therapeutic insights.Cell communication and signaling : CCS · 2024Review
- Gut Microbiota Metabolites: Unveiling Their Role in Inflammatory Bowel Diseases and Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Molecular Foundations of Inflammatory Diseases: Insights into Inflammation and Inflammasomes.Current issues in molecular biology · 2024Review
- Unlocking the power of short-chain fatty acids in ameliorating intestinal mucosal immunity: a new porcine nutritional approach.Frontiers in cellular and infection microbiology · 2024Review
- PepT1-targeted nanodrug based on co-assembly of anti-inflammatory peptide and immunosuppressant for combined treatment of acute and chronic DSS-induced ColitiS.Frontiers in pharmacology · 2024Article
- Pyroptosis: a new insight into intestinal inflammation and cancer.Frontiers in immunology · 2024Review
- Inflammatory bowel disease activity threatens ankylosing spondylitis: implications from Mendelian randomization combined with transcriptome analysis.Frontiers in immunology · 2024Article
- Article
- Gut microbiota and neonatal acute kidney injury biomarkers.Pediatric nephrology (Berlin, Germany) · 2023Review
- Article
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 9 institutions in 6 countries.
Funding
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.
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Registered trials
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.