ArticleThe Journal of experimental medicine2003
Intracellular recognition of lipopolysaccharide by toll-like receptor 4 in intestinal epithelial cells.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 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
112 citing papers in PubMed, 335 citations in OpenAlex.
- Intracellular heat shock protein-70 negatively regulates TLR4 signaling in the newborn intestinal epithelium.Journal of immunology (Baltimore, Md. : 1950) · 2012Trial
- Potential Roles of Escherichia coli in IgA Nephropathy: Evidence, Mechanistic Hypotheses and Microbiota-Targeted Strategies.Microbial biotechnology · 2026Review
- Crosstalk of immunity and metabolism: interaction of toll-like receptors (TLRs) and gut microbiota.Acta diabetologica · 2025Review
- Different infant formulas can activate toll-like receptor 9 in vitro and inhibit interleukin 6 in human primary intestinal epithelial cells.European journal of nutrition · 2024Article
- Article
- Losartan as a Reproposing Therapeutic Agent in Acute Respiratory Distress Syndrome: Modulating Inflammatory Responses and Cytokine Production.International journal of molecular and cellular medicine · 2024Article
- Lipopolysaccharide Stimulates A549 Cell Migration through p-Tyr 42 RhoA and Phospholipase D1 Activity.Biomolecules · 2023Article
- 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
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Review
- Antimicrobial peptides could antagonize uncontrolled inflammationFrontiers in bioengineering and biotechnology · 2022Review
- Intercrypt sentinel macrophages tune antibacterial NF-κB responses in gut epithelial cells via TNF.The Journal of experimental medicine · 2021Article
- Lipopolysaccharide promotes metastasis via acceleration of glycolysis by the nuclear factor-κB/snail/hexokinase3 signaling axis in colorectal cancer.Cancer & metabolism · 2021Article
- Article
- The Lung Microbiome: A Central Mediator of Host Inflammation and Metabolism in Lung Cancer Patients?Cancers · 2020Review
- Cathelicidin-mediated lipopolysaccharide signaling via intracellular TLR4 in colonic epithelial cells evokes CXCL8 production.Gut microbes · 2020Article
- TAK1: a potent tumour necrosis factor inhibitor for the treatment of inflammatory diseases.Open biology · 2020Review
- The lung microbiota: role in maintaining pulmonary immune homeostasis and its implications in cancer development and therapy.Cellular and molecular life sciences : CMLS · 2020Review
- Caspase-11 Non-canonical Inflammasomes in the Lung.Frontiers in immunology · 2020Review
- The Role of Hyaluronan Treatment in Intestinal Innate Host Defense.Frontiers in immunology · 2020Review
52 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor (TLR)4 has recently been shown to reside in the Golgi apparatus of intestinal crypt epithelial m-ICcl2 cells, colocalizing with internalized lipopolysaccharide (LPS). Here we demonstrate that disruption of the integrity of the Golgi apparatus significantly reduced LPS-mediated nuclear factor kappaB activation. Also, the TLR4 adaptor protein MyD88 and the serine/threonine kinase IRAK-1 were rapidly recruited to the Golgi apparatus upon stimulation. LPS-mediated activation required lipid raft formation and intact clathrin-dependent internalization. In contrast to macrophages, prevention of ligand internalization by use of LPS-coated beads significantly impaired recognition by epithelial cells. The localization of TLR4 to the Golgi apparatus was abrogated by expression of a genetically modified form of the TLR4 binding chaperone gp96. Thus, our data provide evidence that in contrast to the situation in macrophages, LPS recognition in intestinal epithelial cells may occur in the Golgi apparatus and require LPS internalization.
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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.