ArticleJournal of molecular histology2014
Disturbance of intraepithelial lymphocytes in a murine model of acute intestinal ischemia/reperfusion.
Article in Journal of molecular histology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Protective effect of ghrelin on intestinal I/R injury in rats.Open medicine (Warsaw, Poland) · 2022Article
- Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice.Scientific reports · 2021Article
- Intestinal Epithelial Cells-Derived Hypoxia-Inducible Factor-1α Is Essential for the Homeostasis of Intestinal Intraepithelial Lymphocytes.Frontiers in immunology · 2019Article
- AhR activation protects intestinal epithelial barrier function through regulation of Par-6.Journal of molecular histology · 2018Article
- The interplay of BMP4 and IL‑7 regulates the apoptosis of intestinal intraepithelial lymphocytes under conditions of ischemia̸reperfusion.International journal of molecular medicine · 2018Article
- Aryl hydrocarbon receptor activation maintained the intestinal epithelial barrier function through Notch1 dependent signaling pathway.International journal of molecular medicine · 2018Article
- DJ-1 promotes survival of human colon cancer cells under hypoxia by modulating HIF-1α expression through the PI3K-AKT pathway.Cancer management and research · 2018Article
- Aryl Hydrocarbon Receptor Activation Modulates Intestinal Epithelial Barrier Function by Maintaining Tight Junction Integrity.International journal of biological sciences · 2018Article
- γδ T cells in homeostasis and host defence of epithelial barrier tissues.Nature reviews. Immunology · 2017Review
- Tumor Necrosis Factor α-Dependent Neutrophil Priming Prevents Intestinal Ischemia/Reperfusion-Induced Bacterial Translocation.Digestive diseases and sciences · 2017Article
- Conventional alpha beta (αβ) T cells do not contribute to acute intestinal ischemia-reperfusion injury in mice.PloS one · 2017Article
- CD8αα TCRαβ Intraepithelial Lymphocytes in the Mouse Gut.Digestive diseases and sciences · 2016Review
- Calcium glycerophosphate preserves transepithelial integrity in the Caco-2 model of intestinal transport.World journal of gastroenterology · 2015Article
- The canonical Notch signaling was involved in the regulation of intestinal epithelial cells apoptosis after intestinal ischemia/reperfusion injury.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Strategically located at the epithelial basolateral surface, intraepithelial lymphocytes (IELs) are intimately associated with epithelial cells and maintain the epithelial barrier integrity. Intestinal ischemia-reperfusion (I/R)-induced acute injury not only damages the epithelium but also affects the mucosal barrier function. Therefore, we hypothesized that I/R-induced mucosal damage would affect IEL phenotype and function. Adult C57BL/6J mice were treated with intestinal I/R or sham. Mice were euthanized at 6 h after I/R, and the small bowel was harvested for histological examination and to calculate the transmembrane resistance. Occludin expression and IEL location were detected through immunohistochemistry. The IEL phenotype, activation, and apoptosis were examined using flow cytometry. Cytokine and anti-apoptosis-associated gene expressions were measured through RT-PCR. Intestinal I/R induced the destruction of epithelial cells and intercellular molecules (occludin), resulting in IEL detachment from the epithelium. I/R also significantly increased the CD8αβ, CD4, and TCRαβ IEL subpopulations and significantly changed IEL-derived cytokine expression. Furthermore, I/R enhanced activation and promoted apoptosis in IELs. I/R-induced acute intestinal mucosal damage significantly affected IEL phenotype and function. These findings provide profound insight into potential IEL-mediated epithelial barrier dysfunction after intestinal I/R.
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