We used mouse intraepithelial lymphocyte hybridomas (IELH) to study the role of adhesion molecules, especially beta 7 integrins, in the adherence of IELH to intestinal epithelial cells. Unstimulated 9.1 gamma delta IELH cells expressed high levels of CD11a, CD11a/CD18, CD44, and CD45; medium levels of CD45RB and integrin alpha 4; low levels of alpha M290, beta 7, and 33D1; and very low levels of ICAM-1 and VCAM-1. PHA and TGF-beta stimulated IELH cells--but not control BW5147 cells (alpha 4/beta 7 integrin negative fusion partner)--to bind to IEC-18 and CMT-93 intestinal epithelial cells, but not to renal mesangial cells. The binding was partially blocked by mAbs to integrin alpha 4 and/or alpha M290. The two mAbs in combination did not completely block the binding, suggesting that epitopes not recognized by these two mAbs are also involved in binding. The adhesion of 9.1 gamma delta cells to IEC-18 cells was also partially inhibited by mAbs to VCAM-1, LFA-1, and CD44, but not by mAbs CD45 and a control rat IgG. Thus, IELH may be a useful model system with which to study the role of adhesion molecules in the interaction between IEL and intestinal epithelial cells.
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http://dx.doi.org/10.1006/cimm.1995.1155 | DOI Listing |
Toxicol Rep
June 2025
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, West Bengal 700054, India.
Colitis is an inflammatory disorder of the gastrointestinal tract. A widely consumed dietary nutrient, α-ketoglutarate (α-KG) is known to play a crucial role in cellular metabolism and provide protection to intestinal epithelium under various pathophysiological conditions. In this study, 2,4,6-trinitrobenzenesulfonic acid (TNBS) was used to induce colitis in Wistar rats.
View Article and Find Full Text PDFRegen Ther
March 2025
Center for Regenerative Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Gastrointestinal (GI) health underpins systemic well-being, yet the complexity of gut physiology poses significant challenges to understanding disease mechanisms and developing effective, personalized therapies. Traditional models often fail to capture the intricate interplay between epithelial, mesenchymal, immune, and neuronal cells that govern gut homeostasis and disease. Over the past five years, advances in organoid technology have created physiologically relevant, three-dimensional GI models that replicate native tissue architecture and function.
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January 2025
School of Health Preservation and Rehabilitation, Chengdu University of TCM, Shierqiao Road, Chengdu, 610075, Sichuan, People's Republic of China.
Despite the established link between chronic high salt diet (HSD) and an increase in gut inflammation, the effect of HSD on the integrity of the intestinal barrier remains understudied. The present study aims to investigate the impact of HSD on the intestinal barrier in rats, encompassing its mechanical, mucous, and immune components. Expression levels of intestinal tight junction proteins and mucin-2 (MUC2) in SD rats were analyzed using immunofluorescence.
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January 2025
Department of Clinical and Molecular Medicine (IKOM), Faculty of Medicine and Health Sciences, NTNU - Norwegian University of Science and Technology, Prinsesse Kristinas gt. 1, Trondheim, 7030, Norway.
Restoration of the intestinal epithelial barrier is crucial for achieving mucosal healing, the therapeutic goal for inflammatory bowel disease (IBD). During homeostasis, epithelial renewal is maintained by crypt stem cells and progenitors that cease to divide as they differentiate into mature colonocytes. Inflammation is a major effector of mucosal damage in IBD and has been found to affect epithelial stemness, regeneration and cellular functions.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
January 2025
Department of Medicine, University of Western Ontario, London, Ontario N6A 5W9, Canada; Verspeeten Family Cancer Centre, London Health Sciences Centre, London, Ontario, Canada. Electronic address:
Background And Aims: Loss of the tumor suppressor gene Apc in Lgr5+ intestinal stem cells results in aberrant Wnt signaling and colonic tumorigenesis. In the setting of injury, however, we and others have also shown that non-stem cells can also give rise to colonic tumors. The mechanism by which inflammation leads to cellular plasticity and cancer, however, remains largely unknown.
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