ArticleInfection and immunity2004
Nod1 is an essential signal transducer in intestinal epithelial cells infected with bacteria that avoid recognition by toll-like receptors.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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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
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.
- Association of NOD1 (CARD4) insertion/deletion polymorphism with susceptibility to IBD: a meta-analysis.World journal of gastroenterology · 2010Pooled it
- Neonatal enteric infection disrupts the microbiota-gut-brain axis through pattern recognition receptors and altered neuroimmune signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Characterization and Immune Function ofBiology · 2026Article
- Regulation of Intestinal Barrier Function and Gut Microbiota by Hot Melt Extrusion-Drug Delivery System-Prepared Mulberry Anthocyanin in an Inflammatory Bowel Disease Model.Pharmaceuticals (Basel, Switzerland) · 2025Article
- NOD1 and NOD2: Essential Monitoring Partners in the Innate Immune System.Current issues in molecular biology · 2024Review
- Review
- The contribution of the intestinal microbiome to immune recovery after HCT.Frontiers in immunology · 2022Review
- Steamed Ginger Extract Exerts Anti-inflammatory Effects inJournal of cancer prevention · 2021Article
- Bartonella henselae Persistence within Mesenchymal Stromal Cells Enhances Endothelial Cell Activation and Infectibility That Amplifies the Angiogenic Process.Infection and immunity · 2021Article
- NLRP12 in innate immunity and inflammation.Molecular aspects of medicine · 2020Review
- Gut microbiota, NLR proteins, and intestinal homeostasis.The Journal of experimental medicine · 2020Review
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- Article
- Inhibitory Effects of Menadione onInternational journal of molecular sciences · 2019Article
- Infectious Threats, the Intestinal Barrier, and Its Trojan Horse: Dysbiosis.Frontiers in microbiology · 2019Review
- Outer Membrane Vesicles From Probiotic and CommensalFrontiers in microbiology · 2018Article
- Emerging Mechanisms of Innate Immunity and Their Translational Potential in Inflammatory Bowel Disease.Frontiers in medicine · 2018Review
- Infection of human intestinal epithelial cells by invasive bacteria activates NF-κB and increases ICAM-1 expression through NOD1.The Korean journal of internal medicine · 2018Article
- Immune Recognition of the Epidemic Cystic Fibrosis Pathogen Burkholderia dolosa.Infection and immunity · 2017Article
- Nucleotide-binding oligomerization domain 1 and gastrointestinal disorders.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor NF-kappaB in human intestinal epithelial cells plays a central role in regulating genes that govern the onset of mucosal inflammatory responses following intestinal microbial infection. Nod1 is a cytosolic pattern recognition receptor in mammalian cells that senses components of microbial peptidoglycans and signals the activation of NF-kappaB. The aim of these studies was to assess the functional importance of Nod1 in activating NF-kappaB and NF-kappaB proinflammatory target genes in human intestinal epithelium. Human colon epithelial cells that constitutively express Nod1 were used as a model intestinal epithelium. These cells do not signal through Toll-like receptor 4 (TLR4) or respond to bacterial lipopolysaccharide, but they express functional TLR5 and interleukin 1 (IL-1) receptors that signal the activation of NF-kappaB in response to bacterial flagellin or IL-1 stimulation. Stable expression of dominant negative (DN) Nod1 in colon epithelial cells prevented IkappaB kinase and NF-kappaB activation in response to infection with enteroinvasive Escherichia coli. In contrast, DN Nod1 did not eliminate IL-1 or flagellin-stimulated NF-kappaB activation. Inhibition of NF-kappaB was accompanied by inhibition of NF-kappaB target genes that provide signals for the mucosal influx of neutrophils during intestinal infection. We conclude that signaling through Nod1 is required for activating NF-kappaB in human intestinal epithelial cells infected with gram-negative enteric bacteria that can bypass TLR activation. Signaling through Nod1 provides the intestinal epithelium with a backup mechanism for rapidly activating innate immunity during infection with a group of highly invasive pathogenic gram-negative bacteria.
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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.