ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Developmental control of the Nlrp6 inflammasome and a substrate, IL-18, in mammalian intestine.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 88 citations in OpenAlex.
- NLR Inflammasomes in Viral Infections: From Molecular Mechanisms to Therapeutic Interventions.Viruses · 2026Review
- NLRP6 as a candidate segmental barrier to carcinogenesis in the human gut: a hypothesis.Frontiers in immunology · 2026Review
- Gastrodin alleviates high fructose-induced podocyte mitochondria-mediated apoptosis by inhibiting NLRP6 to facilitate TRIM7-triggeredInternational journal of biological sciences · 2026Article
- Interleukin-18 binding protein deficiency results in gut microbiota dysbiosis and aggravated diet-induced MASH in mice.JHEP reports : innovation in hepatology · 2026Article
- Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke.Genes & diseases · 2025Article
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- Inflammasomes: novel therapeutic targets for metabolic syndrome?Frontiers in endocrinology · 2025Review
- Molecular mechanisms of emerging inflammasome complexes and their activation and signaling in inflammation and pyroptosis.Immunological reviews · 2025Review
- Inflammasomes: potential therapeutic targets in hematopoietic stem cell transplantation.Cell communication and signaling : CCS · 2024Review
- NLRP inflammasomes in health and disease.Molecular biomedicine · 2024Review
- Role of NLRP3 in Parkinson's disease: Specific activation especially in dopaminergic neurons.Heliyon · 2024Review
- Role of pyroptosis in the pathogenesis of various neurological diseases.Brain, behavior, and immunity · 2024Review
- Decreased expression of the NLRP6 inflammasome is associated with increased intestinal permeability and inflammation in obesity with type 2 diabetes.Cellular and molecular life sciences : CMLS · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023Review
- Role of the inflammasome in insulin resistance and type 2 diabetes mellitus.Frontiers in immunology · 2023Review
- Spotlight on NLRP6 and Tumor Research Situation: A Potential Cancer Participant.Journal of immunology research · 2023Review
- NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease.Therapeutic advances in gastroenterology · 2023Review
- Know your neighbors: microbial recognition at the intestinal barrier and its implications for gut homeostasis and inflammatory bowel disease.Frontiers in cell and developmental biology · 2023Review
- Race between virus and inflammasomes: inhibition or escape, intervention and therapy.Frontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The inflammasome is a multiprotein complex whose formation is triggered when a NOD-like receptor binds a pathogen ligand, resulting in activated caspase-1, which converts certain interleukins (IL-1β, IL-18, and IL-33) to their active forms. There is currently no information on regulation of this system around the time of birth. We employed transcript profiling of fetal rat intestinal and lung RNA at embryonic days 16 (E16) and 20 (E20) with out-of-sample validation using quantitative RT-PCR. Transcript profiling and quantitative RT-PCR demonstrated that transcripts of core components of the NOD-like receptor Nlrp6 inflammasome (Nlrp6, Pycard, Caspase-1) and one of its substrates, IL-18, were increased at E20 compared with E16 in fetal intestine and not lung. Immunohistochemistry demonstrated increased Pycard in intestinal epithelium. Western blotting demonstrated that IL-18 was undetectable at E16, clearly detectable at E20 in its inactive form, and detectable postnatally in both its inactive and active form. Dramatic upregulation of IL-18 was also observed in the fetal sheep jejunum in late gestation (P = 0.006). Transcription factor binding analysis of the rat array data revealed an overrepresentation of nuclear transcription factor binding sites peroxisome proliferator-activated receptor γ (PPAR-γ) and retinoid X receptor-α and chicken ovalbumin upstream promoter transcription factor 1 in the region 1,000 bp upstream of the transcription start site. Rosiglitazone, a PPAR-γ agonist, more than doubled levels of NLRP6 mRNA in human intestinal epithelial (Caco2) cells. These observations provide the first evidence, to our knowledge, linking activity of PPAR-γ to expression of a NOD-like receptor and adds to a growing body of evidence linking pattern recognition receptors of the innate immune system and intestinal colonization.
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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.