ArticleJournal of pediatric surgery2008
Increased expression and internalization of the endotoxin coreceptor CD14 in enterocytes occur as an early event in the development of experimental necrotizing enterocolitis.
Article in Journal of pediatric surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Activation of Wnt signaling by amniotic fluid stem cell-derived extracellular vesicles attenuates intestinal injury in experimental necrotizing enterocolitis.Cell death & disease · 2020Article
- In vitro analysis of antigen induced T cell-monocyte conjugates by imaging flow cytometry.Journal of immunological methods · 2018Article
- Animal models of necrotizing enterocolitis: review of the literature and state of the art.Innovative surgical sciences · 2018Review
- Enteric serotonin and oxytocin: endogenous regulation of severity in a murine model of necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Mincle suppresses Toll-like receptor 4 activation.Journal of leukocyte biology · 2016Article
- Commensal and probiotic bacteria may prevent NEC by maturing intestinal host defenses.Pathophysiology : the official journal of the International Society for Pathophysiology · 2014Article
- Toll-like receptor regulation of intestinal development and inflammation in the pathogenesis of necrotizing enterocolitis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2014Article
- TLRs, SNPs and VLBWs: oh my!Journal of perinatology : official journal of the California Perinatal Association · 2013Article
- Optimization of a whole blood intracellular cytokine assay for measuring innate cell responses to mycobacteria.Journal of immunological methods · 2012Article
- Pathophysiology and treatment of septic shock in neonates.Clinics in perinatology · 2010Review
- Role of innate host defenses in susceptibility to early-onset neonatal sepsis.Clinics in perinatology · 2010Review
- No longer an innocent bystander: epithelial toll-like receptor signaling in the development of mucosal inflammation.Molecular medicine (Cambridge, Mass.)Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe early signaling events in the development of necrotizing enterocolitis (NEC) remain undefined. We have recently shown that the endotoxin (lipopolysaccharide [LPS]) receptor toll-like receptor 4 (TLR4) on enterocytes is critical in the pathogenesis of experimental NEC. Given that the membrane receptor CD14 is known to facilitate the activation of TLR4, we now hypothesize that endotoxemia induces an early upregulation of CD14 in enterocytes and that this participates in the early intestinal inflammatory response in the development of NEC.
methodsIEC-6 enterocytes were treated with LPS (50 microg/mL), and the subcellular localization of CD14 and TLR4 was assessed by confocal microscopy. C57/Bl6 or CD14-/- mice were treated with LPS (5 mg/kg), whereas experimental NEC was induced using a combination of gavage formula feeding and intermittent hypoxia. CD14 expression was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and reverse transcriptase-polymerase chain reaction, and interleukin 6 was quantified by enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction.
resultsExposure of IEC-6 enterocytes to LPS led to an initial, transient increase in CD14 expression. The early increase in CD14 expression was associated with internalization of CD14 to a perinuclear compartment where increased colocalization with TLR4 was noted. The in vivo significance of these findings is suggested as treatment of mice with LPS led to an early increase in CD14 expression in the intestinal mucosa, whereas the persistent endotoxemia of experimental NEC was associated with decreased CD14 expression within enterocytes.
conclusionsLPS signaling in the enterocyte is marked by an early, transient increase in expression of CD14 and redistribution of the receptor. This process may contribute to the early activation of the intestinal inflammatory response that is observed in the development of NEC.
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