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Molecular Research of Epithelial Function and Barrier Dysfunction
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Molecular Research of Epithelial Function and Barrier Dysfunction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 7020

Special Issue Editor

Dr. Fariba Rezaee

E-Mail Website
Guest Editor
Center for Pediatric Pulmonary Medicine, Cleveland Clinic Children’s, Cleveland, OH 44195, USA
Interests: airway epithelial cell biology; barrier structure and function; impact of viral infection on airway epithelial barrier; impact of electronic cigarettes on airway epithelial barrier

Special Issue Information

Dear Colleagues,

Epithelial cells are a key component of the innate immune system by creating barriers to pathogens and allergens. Dysfunction of the epithelial barrier may allow allergens, viruses, bacteria, pollutants, and other pathogens to invade the subepithelial tissues. Disruption of epithelial integrity promotes pro-inflammatory cytokines and immune responses. Understanding the underlying mechanisms is crucial in determining possible therapeutic targets.

This Special Issue aims to highlight the molecular research of epithelial function and barrier dysfunction. In vitro data, animal studies, and clinical observations in all fields of epithelial biology and barrier function are welcome. Likewise, new assays for identifying the state and function of cell junctions are also welcome. We will ensure that the review process will be fair and timely with proactive Guest Editor participation.

Dr. Fariba Rezaee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • epithelial cells
  • actin cytoskeleton
  • viral infection
  • apical junctional complex
  • tight junction
  • adherens junction
  • barrier dysfunction
  • trans-epithelial electrical resistance
  • permeability
  • epithelial barrier

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Published Papers (4 papers)

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Research

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13 pages, 1875 KiB  
Article
Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells
by Sumiko Abe, Norihiro Harada, Yuuki Sandhu, Hitoshi Sasano, Yuki Tanabe, Shoko Ueda, Takayasu Nishimaki, Yoshihiko Sato, Tomohito Takeshige, Sonoko Harada, Hisaya Akiba and Kazuhisa Takahashi
Int. J. Mol. Sci. 2024, 25(21), 11625; https://doi.org/10.3390/ijms252111625 - 29 Oct 2024
Viewed by 1432
Abstract
Steroid-resistant asthma is a common cause of refractory asthma. Type 2 inflammation is the main inflammatory response in asthma, and the mechanism underlying the steroid-resistance of type 2 inflammation has not been completely elucidated. Tumor-necrosis-factor-like apoptosis-inducing factor (TWEAK) and transforming growth factor (TGF)-β1 [...] Read more.
Steroid-resistant asthma is a common cause of refractory asthma. Type 2 inflammation is the main inflammatory response in asthma, and the mechanism underlying the steroid-resistance of type 2 inflammation has not been completely elucidated. Tumor-necrosis-factor-like apoptosis-inducing factor (TWEAK) and transforming growth factor (TGF)-β1 are involved in epithelial–mesenchymal transition (EMT) and the production of thymic stromal lymphopoietin (TSLP) and C-C motif chemokine ligand 5 (CCL5). We herein hypothesize that the combined exposure to TWEAK and TGF-β1 may result in the development of steroid resistance in bronchial epithelial cells. The bronchial epithelial cell line BEAS-2B was cultured with or without TGF-β1 or TWEAK, in the presence or absence of dexamethasone (DEX). The roles of Smad-independent pathways and MAP kinase phosphatase 1 (MKP-1) were also explored. Co-stimulation of TWEAK and TGF-β1 induced E-cadherin reduction, N-cadherin upregulation, and TSLP and CCL5 production, which were not suppressed by DEX. Inhibition of the nuclear factor kappa beta (NF-κB) and mitogen-activated protein kinase pathways downregulated steroid-unresponsive TSLP and CCL5 production, whereas knockdown of MKP-1 improved steroid-unresponsive TSLP production, induced by co-stimulation with TWEAK and TGF-β1. Therefore, co-stimulation with TWEAK and TGF-β1 can induce the steroid-insensitive production of TSLP and CCL5 in the bronchial epithelium and may contribute to airway inflammation. Full article
(This article belongs to the Special Issue Molecular Research of Epithelial Function and Barrier Dysfunction)
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19 pages, 8438 KiB  
Article
Dietary Bacteriophage Administration Alleviates Enterotoxigenic Escherichia coli-Induced Diarrhea and Intestinal Impairment through Regulating Intestinal Inflammation and Gut Microbiota in a Newly Weaned Mouse Model
by Chao Dong, Yan Chen, Minfeng Ding, Yi Liu, Xingping Chen, Yuyong He, Tiande Zou, Jun Chen and Jinming You
Int. J. Mol. Sci. 2024, 25(19), 10736; https://doi.org/10.3390/ijms251910736 - 5 Oct 2024
Cited by 1 | Viewed by 1565
Abstract
This study aimed to investigate the effects of dietary bacteriophage administration on diarrhea and intestinal impairment induced by enterotoxigenic Escherichia coli (ETEC) in a newly weaned mouse model. Forty-four newly weaned C57BL/6 mice were divided into four treatment groups, where they were provided [...] Read more.
This study aimed to investigate the effects of dietary bacteriophage administration on diarrhea and intestinal impairment induced by enterotoxigenic Escherichia coli (ETEC) in a newly weaned mouse model. Forty-four newly weaned C57BL/6 mice were divided into four treatment groups, where they were provided either the control diet or the bacteriophage-supplemented diet, with or without ETEC infection. The results show that the bacteriophage administration resulted in increased body weight, decreased diarrhea score, and improved jejunal histopathology in ETEC-infected mice. The bacteriophage administration enhanced the intestinal barrier function of the ETEC-infected mice, as indicated by the reduced serum DAO level and the increased expression of Claudin-1, Occludin, and ZO-1 at both the mRNA and protein levels in the jejunum. Also, the bacteriophage administration resulted in a decrease in serum TNF-α and IL-1β levels, a down-regulation of TNF-α and IL-6 mRNA levels in the jejunum, and the inhibition of jejunal TLR-4/NF-κB pathway activation induced by ETEC infection. Moreover, the bacteriophage administration increased the levels of acetic acid, propionic acid, butyric acid, and total short-chain fatty acids in the caecum content. The bacteriophage administration increased the Shannon index, increased the abundance of Bacteroidota and Muribaculaceae, and decreased the abundance of Verrucomicrobiota and Akkermansiaceae in the colon contents of the ETEC-infected mice. Spearman’s correlation analysis indicates that the protective effects of bacteriophage on ETEC-induced intestinal impairment, inflammation, and intestinal barrier function are associated with regulating the abundance of Bacteroidota and Muribaculaceae in the colon contents of mice. Collectively, bacteriophage administration alleviates ETEC-induced diarrhea and intestinal impairment through regulating intestinal inflammation and gut microbiota in newly weaned mice. Full article
(This article belongs to the Special Issue Molecular Research of Epithelial Function and Barrier Dysfunction)
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13 pages, 2501 KiB  
Article
10-Eicosanol Alleviates Patulin-Induced Cell Cycle Arrest and Apoptosis by Activating AKT (Protein Kinase B) in Porcine Intestinal Epithelial Cells
by Chae Hyun Lee, Sangsu Shin and Sang In Lee
Int. J. Mol. Sci. 2024, 25(16), 8597; https://doi.org/10.3390/ijms25168597 - 7 Aug 2024
Cited by 1 | Viewed by 1145
Abstract
Patulin (PAT) is a fungal toxin prevalent in apples and apple products and associated with several toxic effects, potentially harming multiple organs, including the kidneys, liver, and colon. However, the precise molecular mechanism through which PAT affects the intestines remains comprehensively unclear. Therefore, [...] Read more.
Patulin (PAT) is a fungal toxin prevalent in apples and apple products and associated with several toxic effects, potentially harming multiple organs, including the kidneys, liver, and colon. However, the precise molecular mechanism through which PAT affects the intestines remains comprehensively unclear. Therefore, this study aims to investigate the molecular effects of PAT on the intestinal epithelium. Gene expression profiling was conducted, hypothesizing that PAT induces cell cycle arrest and apoptosis through the PI3K-Akt signaling pathway. Cell cycle analysis, along with Annexin-V and propidium iodide staining, confirmed that PAT induced G2/M phase arrest and apoptosis in IPEC-J2 cells. Additionally, PAT activated the expression of cell cycle-related genes (CDK1, CCNB1) and apoptosis-related genes (BCL6, CASP9). Treatment with SC79, an AKT activator, mitigated cell cycle arrest and apoptosis. To identify natural products that could mitigate the harmful effects of PAT in small intestinal epithelial cells in pigs, the high-throughput screening of a natural product library was conducted, revealing 10-Eicosanol as a promising candidate. In conclusion, our study demonstrates that 10-Eicosanol alleviates PAT-induced cell cycle arrest and apoptosis in IPEC-J2 cells by activating AKT. Full article
(This article belongs to the Special Issue Molecular Research of Epithelial Function and Barrier Dysfunction)
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Review

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24 pages, 1458 KiB  
Review
Nanoparticles and Airway Epithelial Cells: Exploring the Impacts and Methodologies in Toxicity Assessment
by Claire E. Lee and Fariba Rezaee
Int. J. Mol. Sci. 2024, 25(14), 7885; https://doi.org/10.3390/ijms25147885 - 18 Jul 2024
Viewed by 2154
Abstract
The production of nanoparticles has recently surged due to their varied applications in the biomedical, pharmaceutical, textile, and electronic sectors. However, this rapid increase in nanoparticle manufacturing has raised concerns about environmental pollution, particularly its potential adverse effects on human health. Among the [...] Read more.
The production of nanoparticles has recently surged due to their varied applications in the biomedical, pharmaceutical, textile, and electronic sectors. However, this rapid increase in nanoparticle manufacturing has raised concerns about environmental pollution, particularly its potential adverse effects on human health. Among the various concerns, inhalation exposure to nanoparticles poses significant risks, especially affecting the respiratory system. Airway epithelial cells play a crucial role as the primary defense against inhaled particulate matter and pathogens. Studies have shown that nanoparticles can disrupt the airway epithelial barrier, triggering inflammatory responses, generating reactive oxygen species, and compromising cell viability. However, our understanding of how different types of nanoparticles specifically impact the airway epithelial barrier remains limited. Both in vitro cell culture and in vivo murine models are commonly utilized to investigate nanoparticle-induced cellular responses and barrier dysfunction. This review discusses the methodologies frequently employed to assess nanoparticle toxicity and barrier disruption. Furthermore, we analyze and compare the distinct effects of various nanoparticle types on the airway epithelial barrier. By elucidating the diverse responses elicited by different nanoparticles, we aim to provide insights that can guide future research endeavors in assessing and mitigating the potential risks associated with nanoparticle exposure. Full article
(This article belongs to the Special Issue Molecular Research of Epithelial Function and Barrier Dysfunction)
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