Background: The role of epithelial cells in eosinophilic esophagitis (EoE) is not well understood. In this study, our aim was to isolate, culture, and expand esophageal epithelial cells obtained from patients with or without EoE and characterize differences observed over time in culture.
Methods: Biopsies were obtained at the time of endoscopy from children with EoE or suspected to have EoE. We established patient-derived esophageal epithelial cell (PDEEC) lines utilizing conditional reprogramming methods. We determined integrin profiles, gene expression, MHC class II expression, and reactivity to antigen stimulation.
Results: The PDEECs were found to maintain their phenotype over several passages. There were differences in integrin profiles and gene expression levels in EoE-Active compared to normal controls and EoE-Remission patients. Once stimulated with antigens, PDEECs express MHC class II molecules on their surface, and when co-cultured with autologous T-cells, there is increased IL-6 and TNF-α secretion in EoE-Active patients vs. controls.
Conclusion: We are able to isolate, culture, and expand esophageal epithelial cells from pediatric patients with and without EoE. Once stimulated with antigens, these cells express MHC class II molecules and behave as non-professional antigen-presenting cells. This method will help us in developing an ex vivo, individualized, patient-specific model for diagnostic testing for causative antigens.
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http://dx.doi.org/10.1038/s41390-018-0033-9 | DOI Listing |
Dev Cell
January 2025
Program in Epithelial Biology and Center for Definitive and Curative Medicine, Stanford University, Stanford, CA, USA. Electronic address:
Human pluripotent stem cell-derived tissue engineering offers great promise for designer cell-based personalized therapeutics, but harnessing such potential requires a deeper understanding of tissue-level interactions. We previously developed a cell replacement manufacturing method for ectoderm-derived skin epithelium. However, it remains challenging to manufacture the endoderm-derived esophageal epithelium despite possessing a similar stratified epithelial structure.
View Article and Find Full Text PDFSurg Endosc
January 2025
Department of Gastroenterology, The First Affiliated Hospital of Sun Yat-Sen University, Guangdong, China.
Background: Submucosal tunneling endoscopic resection (STER) is considered an effective, safe and minimally invasive treatment for esophageal subepithelial lesions (SELs) with maximal dilameter less than 3.0 cm, yet its efficacy for lesions over 3.0 cm remains unclear.
View Article and Find Full Text PDFExpert Rev Mol Diagn
January 2025
Department of Electronics and Communication Engineering, IIITDM Kancheepuram, Chennai, India.
Introduction: Cancer ranks as the second most prevalent cause of death worldwide, responsible for approximately 9.6 million deaths annually. Approximately one out of every six deaths is caused by cancer.
View Article and Find Full Text PDFDiagnostics (Basel)
December 2024
Dow Medical College, Dow University of Health Sciences, Karachi 74200, Pakistan.
: Barrett's esophagus (BE), with metaplastic columnar epithelium in the lower esophagus, predisposes patients to esophageal adenocarcinoma (EAC). Despite extensive research, mechanisms underlying BE progression to EAC remain unclear, and no validated biomarkers are available for clinical use. Progastricsin/Pepsinogen-C (PGC), an aspartic proteinase linked to maintaining normal epithelial morphology, is often absent in advanced gastrointestinal malignancies.
View Article and Find Full Text PDFBiomolecules
December 2024
Division of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
In homeostatic conditions, the basal progenitor cells of the esophagus differentiate into a stratified squamous epithelium. However, in the setting of acid exposure or inflammation, there is a marked failure of basal cell differentiation, leading to basal cell hyperplasia. We have previously shown that lysyl oxidase (LOX), a collagen crosslinking enzyme, is upregulated in the setting of allergic inflammation of the esophagus; however, its role beyond collagen crosslinking is unknown.
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