scholarly journals Exam 2: Inflammation and the Intestinal Barrier: Leukocyte–Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair

2016 ◽  
Vol 151 (4) ◽  
pp. e16-e17
Keyword(s):  
Epithelial Cell ◽  
Intestinal Barrier ◽  
Cell Interactions ◽  
Cell Junction ◽  
Mucosal Repair

scholarly journals Inflammation and the Intestinal Barrier: Leukocyte–Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair

2016 ◽  
Vol 151 (4) ◽  
pp. 616-632 ◽  
Author(s):  
Anny-Claude Luissint ◽  
Charles A. Parkos ◽  
Asma Nusrat
Keyword(s):  
Epithelial Cell ◽  
Intestinal Barrier ◽  
Cell Interactions ◽  
Cell Junction ◽  
Mucosal Repair

scholarly journals Gut Microbiota and Intestinal Trans-Epithelial Permeability

2020 ◽  
Vol 21 (17) ◽  
pp. 6402 ◽  
Author(s):  
Bénédicte Allam-Ndoul ◽  
Sophie Castonguay-Paradis ◽  
Alain Veilleux
Keyword(s):  
Epithelial Cell ◽  
Gut Microbiota ◽  
Tight Junctions ◽  
Intestinal Barrier ◽  
Gut Bacteria ◽  
Cell Interactions ◽  
Epithelial Permeability ◽  
Epithelial Stem Cells ◽  
Barrier Functions ◽  
Molecular Aspects

Constant remodeling of tight junctions to regulate trans-epithelial permeability is essential in maintaining intestinal barrier functions and thus preventing diffusion of small molecules and bacteria to host systemic circulation. Gut microbiota dysbiosis and dysfunctional gut barrier have been correlated to a large number of diseases such as obesity, type 2 diabetes and inflammatory bowel disease. This led to the hypothesis that gut bacteria-epithelial cell interactions are key regulators of epithelial permeability through the modulation of tight junctions. Nevertheless, the molecular basis of host-pathogen interactions remains unclear mostly due to the inability of most in vitro models to recreate the differentiated tissue structure and components observed in the normal intestinal epithelium. Recent advances have led to the development of a novel cellular model derived from intestinal epithelial stem cells, the so-called organoids, encompassing all epithelial cell types and reproducing physiological properties of the intestinal tissue. We summarize herein knowledge on molecular aspects of intestinal barrier functions and the involvement of gut bacteria-epithelial cell interactions. This review also focuses on epithelial organoids as a promising model for epithelial barrier functions to study molecular aspects of gut microbiota-host interaction.

scholarly journals Epithelial CD47 is critical for mucosal repair in the murine intestine in vivo

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Michelle Reed ◽  
Anny-Claude Luissint ◽  
Veronica Azcutia ◽  
Shuling Fan ◽  
Monique N. O’Leary ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Wound Repair ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Primary Cultures ◽  
Intestinal Barrier ◽  
Mucosal Repair

Abstract CD47 is a ubiquitously expressed transmembrane glycoprotein that regulates inflammatory responses and tissue repair. Here, we show that normal mice treated with anti-CD47 antibodies, and Cd47-null mice have impaired intestinal mucosal wound healing. Furthermore, intestinal epithelial cell (IEC)-specific loss of CD47 does not induce spontaneous immune-mediated intestinal barrier disruption but results in defective mucosal repair after biopsy-induced colonic wounding or Dextran Sulfate Sodium (DSS)-induced mucosal damage. In vitro analyses using primary cultures of CD47-deficient murine colonic IEC or human colonoid-derived IEC treated with CD47-blocking antibodies demonstrate impaired epithelial cell migration in wound healing assays. Defective wound repair after CD47 loss is linked to decreased epithelial β1 integrin and focal adhesion signaling, as well as reduced thrombospondin-1 and TGF-β1. These results demonstrate a critical role for IEC-expressed CD47 in regulating mucosal repair and raise important considerations for possible alterations in wound healing secondary to therapeutic targeting of CD47.

scholarly journals Colon Epithelial MicroRNA Network in Fatty Liver

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Paule V. Joseph ◽  
Sarah K. Abey ◽  
Dan Wang ◽  
Nicolaas H. Fourie ◽  
Natnael D. Kenea ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Fatty Liver ◽  
Intestinal Barrier ◽  
Signaling Network ◽  
Cell Junctions ◽  
Cell Junction ◽  
Global Changes ◽  
Cell Monolayers ◽  
Epithelial Barriers ◽  
Junction Structure

Background & Aims. Intestinal barrier alterations are associated with fatty liver (FL) and metabolic syndrome (MetS), but microRNA (miR) signaling pathways in MetS-FL pathogenesis remain unclear. This study investigates an epithelial-focused miR network in colorectal cell models based on the previously reported MetS-FL miR trio of hsa-miR-142-3p, hsa-miR-18b, and hsa-miR-890. Methods. Each miR mimic construct of MetS-FL miR trio was transfected into human colorectal cells, CRL-1790 or Caco-2. Global miRNome changes posttransfection were profiled (nCounter® Human v3 miRNA, NanoString Technologies). Changes in barrier (transepithelial electrical resistance, TEER) and epithelial cell junction structure (Occludin and Zona Occludens-1/ZO-1 immunofluorescence staining-confocal microscopy) were examined pre- and posttransfection in Caco-2 cell monolayers. A signaling network was constructed from the MetS-FL miR trio, MetS-FL miR-induced colorectal miRNome changes, ZO-1, and Occludin. Results. Transfection of CRL-1790 cells with each MetS-FL miR mimic led to global changes in the cellular miRNome profile, with 288 miRs being altered in expression by more than twofold. Eleven miRs with known cytoskeletal and metabolic roles were commonly altered in expression by all three miR mimics. Transfection of Caco-2 cell monolayers with each MetS-FL miR mimic induced barrier-associated TEER variations and led to structural modifications of ZO-1 and Occludin within epithelial cell junctions. Pathway analysis incorporating the MetS-FL miR trio, eleven common target miRs, ZO-1, and Occludin revealed a signaling network centered on TNF and AKT2, which highlights injury, inflammation, and hyperplasia. Conclusions. Colon-specific changes in epithelial barriers, cell junction structure, and a miRNome signaling network are described from functional studies of a MetS-FL miR trio signature.

Increased epithelial-free areas in thymuses with altered EphB-mediated thymocyte–thymic epithelial cell interactions

2017 ◽  
Vol 148 (4) ◽  
pp. 381-394 ◽  
Author(s):  
Javier García-Ceca ◽  
Sara Montero-Herradón ◽  
David Alfaro ◽  
Agustín G. Zapata
Keyword(s):  
Epithelial Cell ◽  
Cell Interactions ◽  
Thymic Epithelial Cell

Tu1840 Epithelial Cell Junction Regulation by the Stress-Associated miR-150, miR-335, and miR-142-3p in the Absence or Presence of Chronic Dexamethasone

2016 ◽  
Vol 150 (4) ◽  
pp. S957-S958
Author(s):  
Sarah K. Abey ◽  
Jeffrey Robinson ◽  
Nicolaas H. Fourie ◽  
Dan Wang ◽  
Natnael Kenea ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Junction

scholarly journals Inverse-power-law behavior of cellular motility reveals stromal–epithelial cell interactions in 3D co-culture by OCT fluctuation spectroscopy

Optica ◽  
2015 ◽  
Vol 2 (10) ◽  
pp. 877 ◽  
Author(s):  
Amy L. Oldenburg ◽  
Xiao Yu ◽  
Thomas Gilliss ◽  
Oluwafemi Alabi ◽  
Russell M. Taylor ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Power Law ◽  
Cell Interactions ◽  
Inverse Power ◽  
Cellular Motility ◽  
Inverse Power Law
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