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Regulation and Physiopathology of Gut Barrier
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Regulation and Physiopathology of Gut Barrier

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 32625

Special Issue Editors

Dr. Véronique Carrière

E-Mail Website
Guest Editor
Centre de Recherche Saint-Antoine, INSERM, Sorbonne University, Paris, France
Interests: intestinal inflammation; obesity; intestinal epithelial cells; paracellular permeability; cytokines; intestinal lipid metabolism; bile acids; enterocyte-like Caco-2/TC7 cell line; human and mouse gut organoids
Dr. Sophie Thenet

E-Mail Website
Guest Editor
Centre de Recherche Saint-Antoine, Sorbonne University, EPHE, PSL University, Paris, France
Interests: regulation of cell-cell junctions (adherens junctions, tight junctions, desmosomes) in intestinal epithelial cells and impact on paracellular permeability; intestinal barrier function in metabolic diseases and inflammatory bowel disease

Special Issue Information

Dear Colleagues,

The intestinal barrier refers to chemical and physical components of the intestinal mucosa, which form a dynamic interface between the gut lumen and the body. The intestinal mucosa ensures an efficient equilibrium between the absorption of nutrients and the prevention of uncontrolled translocation of harmful luminal contents such as pathogens or toxins. The integrity of the gut barrier participates to the intestinal homeostasis and is essential for health preservation. Intestinal mucosa barrier dysfunction has been implicated in several pathologies, such as metabolic disorders or inflammatory bowel disease.

Many actors are involved in maintaining an effective gut barrier. The intestinal epithelial cells, through cell-cell contacts and notably the presence of tight junctions, form a physical barrier. Intestinal epithelial cells also contribute to the establishment of a chemical barrier through the secretion into the lumen of mucus, secretory IgA and antimicrobial peptides, which take part in microbiota homeostasis. The immune cells present in the intestinal mucosa act as an immunological defense and are involved in the education of systemic immune system towards commensal microbiota while protecting the gut and the body from intrusion of bacteria and other microorganisms. All these actors are constantly challenged by numerous stimuli originating from either the intestinal lumen or from the blood compartment, such as nutrients, microbiota-derived components and metabolites, cytokines, hormones... Interactions between the different cell types present within the epithelial lining, and more broadly in the intestinal mucosa and submucosa layers including the enteric nervous system, may also affect the gut barrier function.

All aspects of gut barrier regulation and dysfunction throughout life (including developmental aspects, aging) in health and disease are welcome in this special issue, which will take into consideration submissions of both original research articles and reviews.

Dr. Véronique Carrière
Dr. Sophie Thenet
Guest Editors

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

  • Intestinal barrier function
  • Leaky gut
  • Intestinal permeability
  • Cell-cell junctions
  • Inflammation
  • Bacterial metabolites
  • Host microbiota crosstalk
  • Pathogen invasion
  • Nutrients
  • Hormones
  • Cytokines

Published Papers (8 papers)

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Editorial

Jump to: Research, Review

10 pages, 862 KiB  
Editorial
Special Issue on the “Regulation and Physiopathology of the Gut Barrier”
by Sophie Thenet and Véronique Carrière
Int. J. Mol. Sci. 2022, 23(18), 10638; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810638 - 13 Sep 2022
Cited by 1 | Viewed by 1333
Abstract
The importance of gut barrier integrity in intestinal homeostasis and the consequences of its alteration in the etiology of human pathologies have been subjects of exponentially growing interest during the last decade [...] Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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Research

Jump to: Editorial, Review

14 pages, 2979 KiB  
Article
Metformin Protects the Intestinal Barrier by Activating Goblet Cell Maturation and Epithelial Proliferation in Radiation-Induced Enteropathy
by Hyosun Jang, Soyeon Kim, Hyewon Kim, Su Hyun Oh, Seo Young Kwak, Hyun-Woo Joo, Seung Bum Lee, Won Il Jang, Sunhoo Park and Sehwan Shim
Int. J. Mol. Sci. 2022, 23(11), 5929; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23115929 - 25 May 2022
Cited by 18 | Viewed by 2297
Abstract
Radiotherapy or accidental exposure to high-dose radiation can cause severe damage to healthy organs. The gastrointestinal (GI) tract is a radiation-sensitive organ of the body. The intestinal barrier is the first line of defense in the GI tract, and consists of mucus secreted [...] Read more.
Radiotherapy or accidental exposure to high-dose radiation can cause severe damage to healthy organs. The gastrointestinal (GI) tract is a radiation-sensitive organ of the body. The intestinal barrier is the first line of defense in the GI tract, and consists of mucus secreted by goblet cells and a monolayer of epithelium. Intestinal stem cells (ISCs) help in barrier maintenance and intestinal function after injury by regulating efficient regeneration of the epithelium. The Wnt/β-catenin pathway plays a critical role in maintaining the intestinal epithelium and regulates ISC self-renewal. Metformin is the most widely used antidiabetic drug in clinical practice, and its anti-inflammatory, antioxidative, and antiapoptotic effects have also been widely studied. In this study, we investigated whether metformin alleviated radiation-induced enteropathy by focusing on its role in protecting the epithelial barrier. We found that metformin alleviated radiation-induced enteropathy, with increased villi length and crypt numbers, and restored the intestinal barrier function in the irradiated intestine. In a radiation-induced enteropathy mouse model, metformin treatment increased tight-junction expression in the epithelium and inhibited bacterial translocation to mesenteric lymph nodes. Metformin increased the number of ISCs from radiation toxicity and enhanced epithelial repair by activating Wnt/β-catenin signaling. These data suggested that metformin may be a potential therapeutic agent for radiation-induced enteropathy. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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14 pages, 2856 KiB  
Article
Peripheral Opioid Receptor Blockade Enhances Epithelial Damage in Piroxicam-Accelerated Colitis in IL-10-Deficient Mice
by Xavier Mas-Orea, Morgane Sebert, Mehdi Benamar, Camille Petitfils, Catherine Blanpied, Abdelhadi Saoudi, Céline Deraison, Frederick Barreau, Nicolas Cenac and Gilles Dietrich
Int. J. Mol. Sci. 2021, 22(14), 7387; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147387 - 09 Jul 2021
Cited by 6 | Viewed by 2435
Abstract
Mucosal CD4+ T lymphocytes display a potent opioid-mediated analgesic activity in interleukin (IL)-10 knockout mouse model of inflammatory bowel diseases (IBD). Considering that endogenous opioids may also exhibit anti-inflammatory activities in the periphery, we examined the consequences of a peripheral opioid receptor [...] Read more.
Mucosal CD4+ T lymphocytes display a potent opioid-mediated analgesic activity in interleukin (IL)-10 knockout mouse model of inflammatory bowel diseases (IBD). Considering that endogenous opioids may also exhibit anti-inflammatory activities in the periphery, we examined the consequences of a peripheral opioid receptor blockade by naloxone-methiodide, a general opioid receptor antagonist unable to cross the blood–brain barrier, on the development of piroxicam-accelerated colitis in IL-10-deficient (IL-10-/-) mice. Here, we show that IL-10-deficient mice treated with piroxicam exhibited significant alterations of the intestinal barrier function, including permeability, inflammation-related bioactive lipid mediators, and mucosal CD4+ T lymphocyte subsets. Opioid receptor antagonization in the periphery had virtually no effect on colitis severity but significantly worsened epithelial cell apoptosis and intestinal permeability. Thus, although the endogenous opioid tone is not sufficient to reduce the severity of colitis significantly, it substantially contributes to the protection of the physical integrity of the epithelial barrier. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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Review

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28 pages, 923 KiB  
Review
Impact of Epithelial Cell Shedding on Intestinal Homeostasis
by Phuong A. Ngo, Markus F. Neurath and Rocío López-Posadas
Int. J. Mol. Sci. 2022, 23(8), 4160; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23084160 - 09 Apr 2022
Cited by 19 | Viewed by 4094
Abstract
The gut barrier acts as a first line of defense in the body, and plays a vital role in nutrition and immunoregulation. A layer of epithelial cells bound together via intercellular junction proteins maintains intestinal barrier integrity. Based on a tight equilibrium between [...] Read more.
The gut barrier acts as a first line of defense in the body, and plays a vital role in nutrition and immunoregulation. A layer of epithelial cells bound together via intercellular junction proteins maintains intestinal barrier integrity. Based on a tight equilibrium between cell extrusion and cell restitution, the renewal of the epithelium (epithelial turnover) permits the preservation of cell numbers. As the last step within the epithelial turnover, cell shedding occurs due to the pressure of cell division and migration from the base of the crypt. During this process, redistribution of tight junction proteins enables the sealing of the epithelial gap left by the extruded cell, and thereby maintains barrier function. Disturbance in cell shedding can create transient gaps (leaky gut) or cell accumulation in the epithelial layer. In fact, numerous studies have described the association between dysregulated cell shedding and infection, inflammation, and cancer; thus epithelial cell extrusion is considered a key defense mechanism. In the gastrointestinal tract, altered cell shedding has been observed in mouse models of intestinal inflammation and appears as a potential cause of barrier loss in human inflammatory bowel disease (IBD). Despite the relevance of this process, there are many unanswered questions regarding cell shedding. The investigation of those mechanisms controlling cell extrusion in the gut will definitely contribute to our understanding of intestinal homeostasis. In this review, we summarized the current knowledge about intestinal cell shedding under both physiological and pathological circumstances. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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18 pages, 1369 KiB  
Review
Enteroendocrine System and Gut Barrier in Metabolic Disorders
by Céline Osinski, Dounia Moret, Karine Clément, Patricia Serradas and Agnès Ribeiro
Int. J. Mol. Sci. 2022, 23(7), 3732; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073732 - 29 Mar 2022
Cited by 10 | Viewed by 4390
Abstract
With the continuous rise in the worldwide prevalence of obesity and type 2 diabetes, developing therapies regulating body weight and glycemia has become a matter of great concern. Among the current treatments, evidence now shows that the use of intestinal hormone analogs (e.g., [...] Read more.
With the continuous rise in the worldwide prevalence of obesity and type 2 diabetes, developing therapies regulating body weight and glycemia has become a matter of great concern. Among the current treatments, evidence now shows that the use of intestinal hormone analogs (e.g., GLP1 analogs and others) helps to control glycemia and reduces body weight. Indeed, intestinal endocrine cells produce a large variety of hormones regulating metabolism, including appetite, digestion, and glucose homeostasis. Herein, we discuss how the enteroendocrine system is affected by local environmental and metabolic signals. These signals include those arising from unbalanced diet, gut microbiota, and the host metabolic organs and their complex cross-talk with the intestinal barrier integrity. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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26 pages, 748 KiB  
Review
The Epithelial Cell Leak Pathway
by Ashley Monaco, Ben Ovryn, Josephine Axis and Kurt Amsler
Int. J. Mol. Sci. 2021, 22(14), 7677; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147677 - 18 Jul 2021
Cited by 40 | Viewed by 4426
Abstract
The epithelial cell tight junction structure is the site of the transepithelial movement of solutes and water between epithelial cells (paracellular permeability). Paracellular permeability can be divided into two distinct pathways, the Pore Pathway mediating the movement of small ions and solutes and [...] Read more.
The epithelial cell tight junction structure is the site of the transepithelial movement of solutes and water between epithelial cells (paracellular permeability). Paracellular permeability can be divided into two distinct pathways, the Pore Pathway mediating the movement of small ions and solutes and the Leak Pathway mediating the movement of large solutes. Claudin proteins form the basic paracellular permeability barrier and mediate the movement of small ions and solutes via the Pore Pathway. The Leak Pathway remains less understood. Several proteins have been implicated in mediating the Leak Pathway, including occludin, ZO proteins, tricellulin, and actin filaments, but the proteins comprising the Leak Pathway remain unresolved. Many aspects of the Leak Pathway, such as its molecular mechanism, its properties, and its regulation, remain controversial. In this review, we provide a historical background to the evolution of the Leak Pathway concept from the initial examinations of paracellular permeability. We then discuss current information about the properties of the Leak Pathway and present current theories for the Leak Pathway. Finally, we discuss some recent research suggesting a possible molecular basis for the Leak Pathway. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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14 pages, 1188 KiB  
Review
How Can a Polymeric Formula Induce Remission in Crohn’s Disease Patients?
by Kawthar Boumessid, Frederick Barreau and Emmanuel Mas
Int. J. Mol. Sci. 2021, 22(8), 4025; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084025 - 14 Apr 2021
Cited by 5 | Viewed by 2910
Abstract
Crohn’s disease is an inflammatory bowel disease whose prevalence is increasing worldwide. Among medical strategies, dietary therapy with exclusive enteral nutrition is recommended as a first-line option, at least for children, because it induces clinical remission and mucosal healing. Modulen®, a [...] Read more.
Crohn’s disease is an inflammatory bowel disease whose prevalence is increasing worldwide. Among medical strategies, dietary therapy with exclusive enteral nutrition is recommended as a first-line option, at least for children, because it induces clinical remission and mucosal healing. Modulen®, a polymeric TGF-β2 enriched formula, has good palatability and is widely used. For the first time in the literature, this review outlines and discusses the clinical outcomes obtained with this therapy, as well as the potential mechanisms of action of its compounds. It can be explained by its TGF-β2 content, but also by its protein and lipid composition. Further well-designed studies are required to improve our knowledge and to optimize therapeutic strategies. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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20 pages, 3809 KiB  
Review
Tight Junctions as a Key for Pathogens Invasion in Intestinal Epithelial Cells
by Tracy Paradis, Hervé Bègue, Louise Basmaciyan, Frédéric Dalle and Fabienne Bon
Int. J. Mol. Sci. 2021, 22(5), 2506; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052506 - 02 Mar 2021
Cited by 99 | Viewed by 9503
Abstract
Tight junctions play a major role in maintaining the integrity and impermeability of the intestinal barrier. As such, they act as an ideal target for pathogens to promote their translocation through the intestinal mucosa and invade their host. Different strategies are used by [...] Read more.
Tight junctions play a major role in maintaining the integrity and impermeability of the intestinal barrier. As such, they act as an ideal target for pathogens to promote their translocation through the intestinal mucosa and invade their host. Different strategies are used by pathogens, aimed at directly destabilizing the junctional network or modulating the different signaling pathways involved in the modulation of these junctions. After a brief presentation of the organization and modulation of tight junctions, we provide the state of the art of the molecular mechanisms leading to permeability breakdown of the gut barrier as a consequence of tight junctions’ attack by pathogens, including bacteria, viruses, fungi, and parasites. Full article
(This article belongs to the Special Issue Regulation and Physiopathology of Gut Barrier)
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