ArticleThe Journal of experimental medicine2011
Constitutive intestinal NF-κB does not trigger destructive inflammation unless accompanied by MAPK activation.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 85 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
85 citing papers in PubMed, 151 citations in OpenAlex.
- Epithelial TRIM27 Inhibits Intestinal Inflammation in Ulcerative Colitis by the USP7/TRIM27-IKK Double Negative-Feedback.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Local Peritoneal Cytokine Response IL-1β, IL-6, TNF-α in a Standardized Neonatal Rat Model of Necrotizing Enterocolitis.International journal of molecular sciences · 2026Article
- Article
- An NF-kB/TNF-alpha signalling feedback loop acts to coordinate tissue regeneration and macrophage behaviour in zebrafish.NPJ Regenerative medicine · 2025Article
- CO-Releasing Polyoxometalates Nanozyme with Gut Mucosal Immunity and Microbiota Homeostasis Remodeling Effects for Restoring Intestinal Barrier Integrity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Alterations in Signaling Pathways and Therapeutic Strategies of Traditional Chinese Medicine in Granulomatous Lobular Mastitis.Journal of inflammation research · 2025Review
- Platelet transcription factors license the pro-inflammatory cytokine response of human monocytes.EMBO molecular medicine · 2024Article
- Glutamine Supplementation: A Possible Strategy to Help Mitigate Health Risks of Heat-Related Illness.Journal of nutrition and metabolism · 2024Review
- Microbial Metabolites as Ligands to Xenobiotic Receptors: Chemical Mimicry as Potential Drugs of the Future.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Article
- YAP Activates STAT3 Signalling to Promote Colonic Epithelial Cell Proliferation in DSS-Induced Colitis and Colitis Associated Cancer.Journal of inflammation research · 2022Article
- IKBKE-driven TPL2 and MEK1 phosphorylations sustain constitutive ERK1/2 activation in tumor cells.EXCLI journal · 2022Article
- Intercrypt sentinel macrophages tune antibacterial NF-κB responses in gut epithelial cells via TNF.The Journal of experimental medicine · 2021Article
- NF-κB determines Paneth versus goblet cell fate decision in the small intestine.Development (Cambridge, England) · 2021Article
- Chitin Glucan Shifts Luminal and Mucosal Microbial Communities, Improve Epithelial Barrier and Modulates Cytokine Production In Vitro.Nutrients · 2021Article
- NF-kappa-B activation unveils the presence of inflammatory hotspots in human gut xenografts.PloS one · 2021Article
- Activating Transcription Factor 6 Mediates Inflammatory Signals in Intestinal Epithelial Cells Upon Endoplasmic Reticulum Stress.Gastroenterology · 2020Article
- CARD14eLife · 2020Article
- IκBα deficiency imposes a fetal phenotype to intestinal stem cells.EMBO reports · 2020Article
- Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression.Molecular biology reports · 2020Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Nuclear factor (NF)-κB, activated by IκB kinase (IKK), is a key regulator of inflammation, innate immunity, and tissue integrity. NF-κB and one of its main activators and transcriptional targets, tumor necrosis factor (TNF), are up-regulated in many inflammatory diseases that are accompanied by tissue destruction. The etiology of many inflammatory diseases is poorly understood, but often depends on genetic factors and environmental triggers that affect NF-κB and related pathways. It is unknown, however, whether persistent NF-κB activation is sufficient for driving symptomatic chronic inflammation and tissue damage. To address this question, we generated IKKβ(EE)(IEC) mice, which express a constitutively active form of IKKβ in intestinal epithelial cell (IECs). IKKβ(EE)(IEC) mice exhibit NF-κB activation in IECs and express copious amounts of inflammatory chemokines, but only small amounts of TNF. Although IKKβ(EE)(IEC) mice exhibit inflammatory cell infiltration in the lamina propria (LP) of their small intestine, they do not manifest tissue damage. Yet, upon challenge with relatively mild immune and microbial stimuli, IKKβ(EE)(IEC) mice succumb to destructive acute inflammation accompanied by enterocyte apoptosis, intestinal barrier disruption, and bacterial translocation. Inflammation is driven by massive TNF production, which requires additional activation of p38 and extracellular-signal-regulated kinase mitogen-activated protein kinases (MAPKs).
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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.