ArticleShock (Augusta, Ga.)2020
Overexpression of BCL-2 in the Intestinal Epithelium Prevents Sepsis-Induced Gut Barrier Dysfunction via Altering Tight Junction Protein Expression.
Article in Shock (Augusta, Ga.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 72 citations in OpenAlex.
- Article
- Epithelial Gab1 Restricts Sepsis-Induced Intestinal Injury by Orchestrating TNF/NF-κB Axis.Mediators of inflammation · 2026Article
- Hydroxysafflor yellow A attenuates sepsis-induced intestinal barrier dysfunction by modulating Bcl-2/SOD2-mediated mitochondrial apoptosis.Frontiers in pharmacology · 2026Article
- Kidney-organ interactions: recent advances and clinical implications.Current opinion in critical care · 2025Review
- Host stress proteins shape hemorrhagic shock via gut microbiota: evidence from Mendelian randomization and animal models.Journal of translational medicine · 2025Article
- The pasteurized Weissella cibaria alleviates sepsis-induced acute lung injury by modulation of intestinal mucus barrier and gut microbiota.Journal of translational medicine · 2025Article
- Nanocrystalline cellulose-geniposide complex enhances gut-brain axis modulation for depression treatment.Communications biology · 2025Article
- INTESTINAL EPITHELIAL-SPECIFIC OCCLUDIN DELETION WORSENS GUT PERMEABILITY AND SURVIVAL FOLLOWING SEPSIS.Shock (Augusta, Ga.) · 2025Article
- Gut integrity in intensive care: alterations in host permeability and the microbiome as potential therapeutic targets.Journal of intensive care · 2025Review
- A review of gut failure as a cause and consequence of critical illness.Critical care (London, England) · 2025Review
- Feed status and skin injury modulate immunopathology, global gene expression, and survival in channel catfish during virulentFrontiers in immunology · 2025Article
- Hydroxysafflor Yellow A Mitigates Sepsis-Induced Pulmonary and Intestinal Injury by Inhibiting TP53 Mediated Ferroptosis.Infection and drug resistance · 2025Article
- The postbiotic of hawthorn-probiotic ameliorates constipation by multi-pathway inhibition of PANoptosis in intestinal epithelial cells.Frontiers in immunology · 2025Article
- Gut Microbiota and Liver Dysfunction in Sepsis: The Role of Inflammatory Mediators and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Marine red yeast supplementation improves laying performance by regulating small intestinal homeostasis in aging chickens.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gut Microbiome in Sepsis.Surgical infections · 2023Review
- Dynamic changes in the migratory microbial components of colon tissue during different periods of sepsis in an LPS-induced rat model.Frontiers in cellular and infection microbiology · 2023Article
- 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
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Sepsis induces both intestinal hyperpermeability and epithelial apoptosis. While each has been implicated in mediating sepsis mortality, the relationship between these two processes is unclear. We hypothesized that preventing intestinal apoptosis would prevent gut barrier dysfunction. To test this hypothesis, transgenic mice that overexpress the anti-apoptotic protein Bcl-2 in the gut epithelium (Fabpl-Bcl-2 mice) and wild-type (WT) mice were subjected to sham laparotomy or cecal ligation and puncture and orally gavaged with fluorescein isothiocyanate conjugated-dextran (FD-4) 5 h before sacrifice. Serum FD-4 concentration was assayed to measure intestinal permeability, and jejunal tight junctions were assayed for mRNA and protein expression. Baseline FD-4 concentration was similar between WT and Fabpl-Bcl-2 mice. Intestinal permeability increased 6, 12, 24, and 48 h following sepsis in WT mice; however, FD-4 concentration was significantly lower at each timepoint in Fabpl-Bcl-2 mice. In addition, there were no statistically significant changes in permeability between septic and sham transgenic mice. Intestinal mRNA expression of claudin 3, claudin 5, and occludin was lower in septic Fabpl-Bcl-2 mice, while claudin 4 mRNA levels were higher in Fabpl-Bcl-2 mice. In contrast, no differences were detected in claudins 2, 7, 15, JAM-A, or ZO-1. Protein levels followed the same trend for all tight junction mediators different between WT and Fabpl-Bcl-2 mice except occludin was significantly higher in transgenic mice. Together these results demonstrate that decreasing intestinal epithelial apoptosis prevents hyperpermeability following sepsis via tight junction alterations which may be at least partially responsible for improved survival conferred by Bcl-2 overexpression.
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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.