The Role of Intestinal Epithelial Cells and Their Cellular Interactions

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 4544

Special Issue Editor


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Guest Editor
Department of Animal and Avian Sciences, University of Maryland, College Park, MD, USA
Interests: mucosal barrier, tight and adherens junctions, intestinal stem cells, mesenchymal stromal cells, and postnatal intestinal development

Special Issue Information

Dear Colleagues,

This Special Issue, “The Role of Intestinal Epithelial Cells and their Cellular Interactions”, will mainly focus on the role of intestinal epithelial cells (IECs) and their regulation and crosstalk with stromal and immune cells.

The intestinal mucosal barrier represents the largest interface between the luminal contents and the body's internal milieu. Single-layered IECs are a semipermeable barrier that allows the absorption of nutrients and transport of substances and prevents the entry of harmful substances, luminal antigens, and pathogens. Due to the harsh luminal environment, IECs possess a great capacity for self-renewal to maintain organ homeostasis and promote regeneration, which is fueled by a population of intestinal stem cells. The IECs dynamically interact with both intestinal stromal and immune cells to maintain tissue homeostasis and alterations to pathological conditions. Understanding the impact of IECs and their interaction with subepithelial cells is essential for improving gut health.

We cordially invite authors to submit original research or review articles pertaining to this important and fast-progressing field of biomedicine. Potential topics include, but are not limited to:

 

  • The mucosal barrier in gastrointestinal physiology and pathology;
  • Intestinal stem cell biology in tissue homeostasis and regeneration;
  • The crosstalk of intestinal epithelial cells with stromal or immune cells.

Dr. Younggeon Jin
Guest Editor

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Keywords

  • intestinal epithelial barrier
  • tight junctions
  • intestinal stem cells
  • mesenchymal stromal cells
  • immune cells

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Published Papers (3 papers)

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Research

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12 pages, 1222 KiB  
Article
Hyperosmotic Stress Induces the Expression of Organic Osmolyte Transporters in Porcine Intestinal Cells and Betaine Exerts a Protective Effect on the Barrier Function
by Elena De Angelis, Paolo Borghetti, Benedetta Passeri, Valeria Cavalli, Luca Ferrari, Melania Andrani, Paolo Martelli and Roberta Saleri
Biomedicines 2024, 12(10), 2391; https://doi.org/10.3390/biomedicines12102391 - 18 Oct 2024
Viewed by 620
Abstract
Background/objectives: The porcine intestinal epithelium plays a fundamental role as a defence interface against pathogens. Its alteration can cause severe inflammatory conditions and diseases. Hyperosmotic stress under physiological conditions and upon pathogen challenge can cause malabsorption. Different cell types counteract the osmolarity increase [...] Read more.
Background/objectives: The porcine intestinal epithelium plays a fundamental role as a defence interface against pathogens. Its alteration can cause severe inflammatory conditions and diseases. Hyperosmotic stress under physiological conditions and upon pathogen challenge can cause malabsorption. Different cell types counteract the osmolarity increase by accumulating organic osmolytes such as betaine, taurine, and myo-inositol through specific transporters. Betaine is known for protecting cells from hyperosmotic stress and has positive effects when fed to pigs. The aim of this study is to demonstrate the modulation of osmolyte transporters gene expression in IPEC-J2 during osmolarity changes and assess the effects of betaine. Methods: IPEC-J2 were seeded in transwells, where differentiate as a polarized monolayer. Epithelial cell integrity (TEER), oxidative stress (NO) and gene expression of osmolyte transporters, tight junction proteins (TJp) and pro-inflammatory cytokines were evaluated. Results: Cells treated with NaCl hyperosmolar medium (500 mOsm/L) showed a TEER decrease at 3 h and detachment within 24 h, associated with an osmolyte transporters reduction. IPEC-J2 treated with mannitol hyperosmolar medium (500 mOsm/L) upregulated taurine (TauT), myo-inositol (SMIT) and betaine (BGT1) transporters expression. A decrease in TJp expression was associated with a TEER decrease and an increase in TNFα, IL6, and IL8. Betaine could attenuate the hyperosmolarity-induced reduction in TEER and TJp expression, the NO increase and cytokines upregulation. Conclusions: This study demonstrates the expression of osmolyte transporters in IPEC-J2, which was upregulated upon hyperosmotic treatment. Betaine counteracts changes in intracellular osmolarity by contributing to maintaining the epithelial barrier function and reducing the inflammatory condition. Compatible osmolytes may provide beneficial effects in therapies for diseases characterized by inflammation and TJp-related dysfunctions. Full article
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Review

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19 pages, 1513 KiB  
Review
Subepithelial Stromal Cells: Their Roles and Interactions with Intestinal Epithelial Cells during Gut Mucosal Homeostasis and Regeneration
by Hammed Ayansola, Edith J. Mayorga and Younggeon Jin
Biomedicines 2024, 12(3), 668; https://doi.org/10.3390/biomedicines12030668 - 17 Mar 2024
Viewed by 1724
Abstract
Intestinal epithelial cell activities during homeostasis and regeneration are well described, but their potential interactions with stromal cells remain unresolved. Exploring the functions of these heterogeneous intestinal mesenchymal stromal cells (iMSCs) remains challenging. This difficulty is due to the lack of specific markers [...] Read more.
Intestinal epithelial cell activities during homeostasis and regeneration are well described, but their potential interactions with stromal cells remain unresolved. Exploring the functions of these heterogeneous intestinal mesenchymal stromal cells (iMSCs) remains challenging. This difficulty is due to the lack of specific markers for most functionally homogenous subpopulations. In recent years, however, novel clustering techniques such as single-cell RNA sequencing (scRNA-seq), fluorescence-activated cell sorting (FACS), confocal microscope, and computational remodeling of intestinal anatomy have helped identify and characterize some specific iMSC subsets. These methods help researchers learn more about the localization and functions of iMSC populations during intestinal morphogenic and homeostatic conditions. Consequently, it is imperative to understand the cellular pathways that regulate their activation and how they interact with surrounding cellular components, particularly during intestinal epithelial regeneration after mucosal injury. This review provides insights into the spatial distribution and functions of identified iMSC subtypes. It focuses on their involvement in intestinal morphogenesis, homeostasis, and regeneration. We reviewed related signaling mechanisms implicated during epithelial and subepithelial stromal cell crosstalk. Future research should focus on elucidating the molecular intermediates of these regulatory pathways to open a new frontier for potential therapeutic targets that can alleviate intestinal mucosa-related injuries. Full article
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Other

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8 pages, 2520 KiB  
Brief Report
Colitis Is Associated with Loss of the Histidine Phosphatase LHPP and Upregulation of Histidine Phosphorylation in Intestinal Epithelial Cells
by Markus Linder, Dritan Liko, Venkatesh Kancherla, Salvatore Piscuoglio and Michael N. Hall
Biomedicines 2023, 11(8), 2158; https://doi.org/10.3390/biomedicines11082158 - 1 Aug 2023
Cited by 6 | Viewed by 1511
Abstract
Protein histidine phosphorylation (pHis) is a posttranslational modification involved in cell cycle regulation, ion channel activity and phagocytosis. Using novel monoclonal antibodies to detect pHis, we previously reported that the loss of the histidine phosphatase LHPP (phospholysine phosphohistidine inorganic pyrophosphate phosphatase) results in [...] Read more.
Protein histidine phosphorylation (pHis) is a posttranslational modification involved in cell cycle regulation, ion channel activity and phagocytosis. Using novel monoclonal antibodies to detect pHis, we previously reported that the loss of the histidine phosphatase LHPP (phospholysine phosphohistidine inorganic pyrophosphate phosphatase) results in elevated pHis levels in hepatocellular carcinoma. Here, we show that intestinal inflammation correlates with the loss of LHPP in dextran sulfate sodium (DSS)-treated mice and in inflammatory bowel disease (IBD) patients. Increased histidine phosphorylation was observed in intestinal epithelial cells (IECs), as determined by pHis immunofluorescence staining of colon samples from a colitis mouse model. However, the ablation of Lhpp did not cause increased pHis or promote intestinal inflammation under physiological conditions or after DSS treatment. Our observations suggest that increased histidine phosphorylation plays a role in colitis, but the loss of LHPP is not sufficient to increase pHis or to cause inflammation in the intestine. Full article
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