ArticleCritical care medicine2013
Inhibition of IKKβ in enterocytes exacerbates sepsis-induced intestinal injury and worsens mortality.
Article in Critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 77 citations in OpenAlex.
- Unveiling Gut Homeostasis Disruption in Sepsis: Towards an Integrated Mechanistic and Translational Roadmap.Cell proliferation · 2026Review
- Epithelial Gab1 Restricts Sepsis-Induced Intestinal Injury by Orchestrating TNF/NF-κB Axis.Mediators of inflammation · 2026Article
- Identification of a muropeptide precursor transporter from gut microbiota and its role in preventing intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- circFLNA promotes intestinal injury during abdominal sepsis through Fas-mediated apoptosis pathway by sponging miR-766-3p.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- PTX3 Protects Intestinal Mucosal Barrier Damage in Sepsis Through Toll-Like Receptor Signaling Pathway.Inflammation · 2022Article
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
- Inhibition of visfatin alleviates sepsis-induced intestinal damage by inhibiting Hippo signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- mScience advances · 2022Article
- Article
- Computational prediction of intracellular targets of wild-type or mutant vesicular stomatitis matrix protein.PloS one · 2022Article
- Upregulation of the microRNA rno-miR-146b-5p may be involved in the development of intestinal injury through inhibition of Kruppel-like factor 4 in intestinal sepsis.Bioengineered · 2020Article
- Use of Organ Dysfunction as a Primary Outcome Variable Following Cecal Ligation and Puncture: Recommendations for Future Studies.Shock (Augusta, Ga.) · 2020Article
- Cell death of intestinal epithelial cells in intestinal diseases.Sheng li xue bao : [Acta physiologica Sinica] · 2020Review
- An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea.Clinical science (London, England : 1979) · 2020Article
- Esmolol inhibits inflammation and apoptosis in the intestinal tissue via the overexpression of NF-κB-p65 in the early stage sepsis rats.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020Article
- MicroRNA-674-5p induced by HIF-1α targets XBP-1 in intestinal epithelial cell injury during endotoxemia.Cell death discovery · 2020Article
- Article
- Gut integrity in critical illness.Journal of intensive care · 2019Review
- Cx43 Inhibition Attenuates Sepsis-Induced Intestinal Injury via Downregulating ROS Transfer and the Activation of the JNK1/Sirt1/FoxO3a Signaling Pathway.Mediators of inflammation · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesNuclear factor-κB is a critical regulator of cell-survival genes and the host inflammatory response. The purpose of this study was to investigate the role of enterocyte-specific NF-kB in sepsis through selective ablation of IkB kinase.
designProspective, randomized controlled study.
settingAnimal laboratories in university medical centers. SUBJECTS AND
interventionsMice lacking functional NF-kB in their intestinal epithelium (Vil-Cre/Ikkβ) and wild-type mice were subjected to sham laparotomy or cecal ligation and puncture. Animals were killed at 24 hours or followed 7 days for survival. MEASUREMENTS AND MAIN
resultsSeptic wild-type mice had decreased villus length compared with sham mice, whereas villus atrophy was further exacerbated in septic Vil-Cre/Ikkβ mice. Sepsis induced an increase in intestinal epithelial apoptosis compared with sham mice, which was further exacerbated in Vil-Cre/Ikkβ mice. Sepsis induced intestinal hyperpermeability in wild-type mice compared with sham mice, which was further exacerbated in septic Vil-Cre/Ikkβ mice. This was associated with increased intestinal expression of claudin-2 in septic wild-type mice, which was further increased in septic Vil-Cre/Ikkβ mice. Both, pro-inflammatory and anti-inflammatory cytokines were increased in serum following cecal ligation and puncture, and interleukin 10 and monocyte chemoattractant protein-1 levels were higher in septic Vil-Cre/Ikkβ mice than in septic wild-type mice. All septic mice were bacteremic, but no differences in bacterial load were identified between wild-type and Vil-Cre/Ikkβ mice. To determine the functional significance of these results, animals were followed for survival. Septic wild-type mice had lower mortality than septic Vil-Cre/Ikkβ mice (47% vs 80%, p<0.05). Antitumor necrosis factor administration decreased intestinal apoptosis, permeability, and mortality in wild-type septic mice, and a similar improvement in intestinal integrity and survival were seen when antitumor necrosis factor was given to Vil-Cre/Ikkβ mice.
conclusionsEnterocyte-specific NF-kB has a beneficial role in sepsis by partially preventing sepsis-induced increases in apoptosis and permeability, which are associated with worsening mortality.
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Registered trials
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