ArticlePloS one2010
Platelet-activating factor induces TLR4 expression in intestinal epithelial cells: implication for the pathogenesis of necrotizing enterocolitis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
- Lactate, mean platelet volume, and nSOFA as combined predictors of perforated necrotizing enterocolitis and mortality in preterm infants: a retrospective cohort study.Annals of medicine · 2026Article
- The gut-brain ConNECtion: exploring the developmental impact of necrotizing enterocolitis on the neonatal brain.Pediatric research · 2026Review
- The microbiome's hidden influence: preclinical insights into inflammatory responses in necrotizing enterocolitis.Seminars in immunopathology · 2025Review
- Role of TLR4 in Enteric Glia Response to Clostridioides Difficile Toxins: Insights From In Vivo and In Vitro Studies.Journal of cellular and molecular medicine · 2025Article
- Metabolomics in NEC: An Updated Review.Metabolites · 2023Review
- Intestine and brain TLR-4 modulation following N-acetyl-cysteine treatment in NEC rodent model.Scientific reports · 2023Article
- A bacterial autotransporter impairs innate immune responses by targeting the transcription factor TFE3.Nature communications · 2023Article
- Necrotizing enterocolitis in premature infants-A defect in the brakes? Evidence from clinical and animal studies.Mucosal immunology · 2023Review
- 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
- Recent advances in our understanding of NEC diagnosis, prognosis and surgical approach.Frontiers in pediatrics · 2023Review
- miRNA-21 plays an important role in necrotizing enterocolitis.Archives of medical science : AMS · 2022Article
- Review
- Toll-Like Receptor-4 Antagonist (+)-Naltrexone Protects Against Carbamyl-Platelet Activating Factor (cPAF)-Induced Preterm Labor in Mice.The American journal of pathology · 2020Article
- Targeting Toll-like receptor-4 to tackle preterm birth and fetal inflammatory injury.Clinical & translational immunology · 2020Review
- Preterm neonatal immunology at the intestinal interface.Cellular and molecular life sciences : CMLS · 2020Review
- Impact of Toll-Like Receptor 4 Signaling in Necrotizing Enterocolitis: The State of the Science.Clinics in perinatology · 2019Review
- Fat composition in infant formula contributes to the severity of necrotising enterocolitis.The British journal of nutrition · 2018Article
- Vitamin D ameliorates neonatal necrotizing enterocolitis via suppressing TLR4 in a murine model.Pediatric research · 2018Article
- Cilostazol disrupts TLR-4, Akt/GSK-3β/CREB, and IL-6/JAK-2/STAT-3/SOCS-3 crosstalk in a rat model of Huntington's disease.PloS one · 2018Article
- Pathogenesis of NEC: Role of the innate and adaptive immune response.Seminars in perinatology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a leading cause of morbidity and mortality in neonatal intensive care units, however its pathogenesis is not completely understood. We have previously shown that platelet activating factor (PAF), bacteria and TLR4 are all important factors in the development of NEC. Given that Toll-like receptors (TLRs) are expressed at low levels in enterocytes of the mature gastrointestinal tract, but were shown to be aberrantly over-expressed in enterocytes in experimental NEC, we examined the regulation of TLR4 expression and signaling by PAF in intestinal epithelial cells using human and mouse in vitro cell lines, and the ex vivo rat intestinal loop model. In intestinal epithelial cell (IEC) lines, PAF stimulation yielded upregulation of both TLR4 mRNA and protein expression and led to increased IL-8 secretion following stimulation with LPS (in an otherwise LPS minimally responsive cell line). PAF stimulation resulted in increased human TLR4 promoter activation in a dose dependent manner. Western blotting and immunohistochemical analysis showed PAF induced STAT3 phosphorylation and nuclear translocation in IEC, and PAF-induced TLR4 expression was inhibited by STAT3 and NFκB Inhibitors. Our findings provide evidence for a mechanism by which PAF augments inflammation in the intestinal epithelium through abnormal TLR4 upregulation, thereby contributing to the intestinal injury of NEC.
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