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Intestinal organoids are advanced cellular models, which are widely used in mammalian studies to mimic and study in vivo intestinal function and host-pathogen interactions. Growth factors WNT3 and RSPO1 are crucial for the growth of intestinal organoids. Chicken intestinal organoids are currently cultured with mammalian Wnt3a and Rspo1, however, maintaining their longevity has shown to be challenging. Based on the limited homology between mammalian and avian RSPO1, we expect that chicken-derived factors are required for the organoid cultures. Isolated crypts from embryonic tissue of laying hens were growing in the presence of chicken WNT3 and RSPO1, whereas growth in the presence of mammalian Wnt3a and Rspo1 was limited. Moreover, the growth was increased by using Prostaglandin E2 (PGE) and a Forkhead box O1-inhibitor (FOXO1-inhibitor), allowing to culture these organoids for 15 passages. Furthermore, stem cells maintained their ability to differentiate into goblets, enterocytes and enteroendocrine cells in 2D structures. Overall, we show that chicken intestinal organoids can be cultured for multiple passages using chicken-derived WNT3 and RSPO1, PGE, and FOXO1-inhibitor.
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http://dx.doi.org/10.1038/s41598-022-14875-7 | DOI Listing |
Food Res Int
November 2025
Medical School of Nantong University, Nantong 226001, China. Electronic address:
Food nutrition and safety are fundamental to the food industry, and the development of appropriate research models is crucial. Unlike traditional animal models, the innovative organoid/organ-on-a-chip model possess distinct human-like characteristics and genomic stability, which have garnered significant attention in food research. In this review, we conduct a comparative analysis between organoids and traditional animal and 2D cell models.
View Article and Find Full Text PDFJ Microbiol Biotechnol
September 2025
Environmental Diseases Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea.
Enterohemorrhagic (EHEC), a pathotype within the Shiga toxin-producing (STEC) group, is a major etiological agent of severe gastrointestinal illness and life-threatening sequelae, including hemolytic uremic syndrome. Although insights into EHEC pathogenesis have been gained through traditional 2D cell culture systems and animal models, these platforms are limited in their ability to recapitulate human-specific physiological responses and tissue-level interactions. Recent progress in three-dimensional (3D) cell culture systems, such as spheroids, organoids, and organ-on-a-chip (OoC) technologies, has enabled more physiologically relevant models for investigating host-pathogen dynamics.
View Article and Find Full Text PDFInflamm Bowel Dis
September 2025
Gut Microbes and Health Programme, Quadram Institute Bioscience, Norwich Research Park, Norwich, United Kingdom.
Background: Intestinal cells receive incoming signals from neighboring cells and microbial communities. Upstream signaling pathways transduce these signals to reach transcription factors (TFs) that regulate gene expression. In inflammatory bowel disease (IBD), most single nucleotide polymorphisms (SNPs) are in non-coding genomic regions containing TF binding sites.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
September 2025
GenPhySE, Université de Toulouse, INRAE, ENVT, 31326, Castanet Tolosan, France. Electronic address:
Background & Aims: The suckling-to-weaning dietary transition is a key step in intestinal development. The aim of our study was to identify the transcriptome changes induced in each cell type of the intestinal epithelium at the onset of solid food ingestion.
Methods: We compared the single-cell transcriptome of epithelial cells isolated from the caecum of age-matched littermate suckling male rabbits ingesting or not solid food.
Biochem Biophys Res Commun
August 2025
Department of General Surgery, Jinling Clinical Medical College, Nanjing Medical University, Nanjing City, Jiangsu Province, China. Electronic address:
Background: Ulcerative colitis (UC) is a long-lasting, nonspecific inflammatory bowel disease involving continuous, diffuse intestinal mucosal injury. The pathogenesis of UC involves genetic polymorphism, oxidative stress, immune response, and microbial infection. Ferroptosis participates in UC progression as a novel non-apoptotic cell death, and its specific mechanism in UC progression deserves further investigation.
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