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Cells
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Epithelial–Immune Cell Interactions in Gut Homeostasis and Inflammation
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Epithelial–Immune Cell Interactions in Gut Homeostasis and Inflammation

A Special Issue of Cells (ISSN 2073-4409) belonging to the section "Cellular Immunology".

Deadline for manuscript submissions: 10 December 2026 | Viewed by 2194

Editor

Dr. Neeraj Kapur

E-Mail Website
Guest Editor
Department of Internal Medicine, College of Medicine, University of Kentucky, 800 Rose St., MN649, Lexington, KY 40536, USA
Interests: inflammatory bowel diseases; mitochondrial physiology

Special Issue Information

Dear Colleagues,

The intestinal epithelium and mucosal immune system closely coordinate to sustain gut homeostasis and provide effective defenses against injury and infection. Epithelial cells serve as both a physical barrier and as dynamic communicators with various immune cell populations. This intricate epithelial–immune crosstalk preserves tissue health, regulates immune tolerance, and orchestrates protective responses against pathogens. The disruption of these interactions can result in barrier dysfunction, intestinal inflammation, dysbiosis, and disease, including inflammatory bowel disease and colorectal cancer. This Special Issue, “Epithelial-Immune Cell Interactions in Gut Homeostasis and Inflammation”, seeks to showcase emerging insights into the signaling pathways, immune crosstalk, and host–microbe interactions that define mucosal health and welcomes submissions that reveal their molecular and cellular mechanisms, the role of the gut microbiome, the effects of barrier breakdown, and the use of advanced models or technologies to investigate these networks. Reviews and perspectives on strategies that target epithelial–immune cell interactions for therapeutic benefit are also encouraged.

Dr. Neeraj Kapur
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gut homeostasis
  • epithelial barrier
  • immune cell crosstalk
  • barrier dysfunction
  • intestinal inflammation
  • microbiota
  • dysbiosis

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Published Papers (2 papers)

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Research

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27 pages, 4176 KB  
Article
Crypt-Level Tight Junction Remodeling Is Associated with Disease Course and Clinical Outcomes in Inflammatory Bowel Disease
by Efthymios P. Tsounis, Christina Geramoutsou, Ploutarchos Pastras, Ioanna Aggeletopoulou, Pinelopi Bosgana, Theoni Lourida, Georgia Diamantopoulou, Sofia Ritsatou, Efthymios Koniaris, Gerassimos J. Mantzaris, Vasiliki Zolota, Stelios F. Assimakopoulos, Vasiliki Bravou, Konstantinos Thomopoulos, Georgios Theocharis and Christos Triantos
Cells 2026, 15(8), 695; https://doi.org/10.3390/cells15080695 - 15 Apr 2026
Cited by 1 | Viewed by 1050
Abstract
Background: Intestinal barrier dysfunction is a hallmark of inflammatory bowel disease (IBD), yet the clinical significance of tight junction (TJ) remodeling remains unclear. We investigated whether alterations in the expression and localization of key TJ proteins are associated with disease activity and clinical [...] Read more.
Background: Intestinal barrier dysfunction is a hallmark of inflammatory bowel disease (IBD), yet the clinical significance of tight junction (TJ) remodeling remains unclear. We investigated whether alterations in the expression and localization of key TJ proteins are associated with disease activity and clinical outcomes in IBD. Methods: This retrospective, single-center study included patients with Crohn’s disease (CD; n = 100), ulcerative colitis (UC; n = 120), and healthy controls (n = 80). Immunohistochemistry was used to assess the expression and subcellular localization of occludin and claudin-1 separately in surface (SE) and crypt epithelium (CR), with staining classified as predominantly membranous (regular) or cytoplasmic (irregular). The primary endpoint was IBD-related hospitalization. Secondary endpoints included surgery, initiation of biologic therapy, and clinical relapse. Logistic and Cox regression models were applied, and longitudinal changes were assessed in paired biopsies. Results: Both occludin and claudin-1 were dysregulated in active disease, showing increased expression and cytoplasmic redistribution compared with remission and controls. TJ alterations were more pronounced in the CR and correlated with clinical, endoscopic, and histological activity. In CD, occludin CR overexpression was independently associated with hospitalization (aOR 1.010; p = 0.05) and surgery (aHR 1.013; p = 0.005), while irregular occludin CR staining was associated with initiation of biologic therapy (aOR 3.48; p = 0.03). In UC, increased occludin CR levels and irregular CR staining were associated with IBD-related hospitalization in multivariable analyses (aOR 1.014; p = 0.035 and aOR 2.78; p = 0.032, respectively). Higher occludin CR levels identified UC patients at increased risk of clinical relapse (aHR 1.012; p = 0.002). In paired biopsies (n = 127), TJ architecture—particularly in the CR—improved over time, with reduced expression and a shift toward membranous localization, most prominently in bio-experienced patients. Conclusions: TJ remodeling, particularly crypt-level occludin dysregulation, is associated with disease activity and clinical outcomes, capturing a clinically relevant dimension of epithelial barrier dysfunction in IBD. Full article
(This article belongs to the Special Issue Epithelial–Immune Cell Interactions in Gut Homeostasis and Inflammation)
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Review

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13 pages, 1365 KB  
Review
Regenerative Inflammation in IBD: How Type I Interferons and TNF Cross-Talk Converts Epithelial Repair into Therapeutic Response
by Emelia A. M. Hinton, Roslyn A. Kemp, Michael Schultz and Safina Gadeock
Cells 2026, 15(13), 1144; https://doi.org/10.3390/cells15131144 - 24 Jun 2026
Viewed by 664
Abstract
Inflammatory bowel diseases (IBD) are increasingly recognized as disorders in which epithelial dysfunction and maladaptive regeneration may be as important as immune dysregulation. Tumor necrosis factor (TNF), a key mediator of intestinal inflammation and a therapeutic target, plays a dual role in both [...] Read more.
Inflammatory bowel diseases (IBD) are increasingly recognized as disorders in which epithelial dysfunction and maladaptive regeneration may be as important as immune dysregulation. Tumor necrosis factor (TNF), a key mediator of intestinal inflammation and a therapeutic target, plays a dual role in both immune activation and epithelial repair by regulating progenitor cell expansion, lineage plasticity, and chemokine signaling in the intestinal epithelium. During acute injury, TNF-associated responses are generally considered adaptive, supporting crypt repair, barrier restitution, and secretory remodeling pathways. However, in chronic disease, persistent TNF exposure, potentially reinforced by type I interferons (IFN-I), may contribute to the persistence of epithelial regenerative pathways. IFN-I signaling has been suggested in experimental and translational studies to reinforce chemokine networks and transcriptional imprinting. We propose that this potentially converts physiological repair into a sustained state of what we have termed “regenerative inflammation,” in which epithelial-derived signals may perpetuate immune recruitment and tissue remodeling. Such TNF-IFN-imprinted epithelial states may contribute to sustained pathology in a subset of patients and could be associated with reduced responsiveness to anti-TNF therapy, although direct causal evidence in human disease remains limited. By integrating mechanistic, organoid-based, and clinical observational evidence, we propose that chronic TNF–IFN crosstalk may contribute to a self-sustaining regenerative inflammatory circuit, providing a conceptual framework for disease persistence in IBD and highlighting potential opportunities to target epithelial-immune interactions. Full article
(This article belongs to the Special Issue Epithelial–Immune Cell Interactions in Gut Homeostasis and Inflammation)
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