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Cells
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The Gut-Liver Crosstalk in Liver Disease
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The Gut-Liver Crosstalk in Liver Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 11201

Special Issue Editor

Prof. Dr. Lindsey Devisscher

E-Mail Website
Guest Editor
Gut–Liver ImmunoPharmacology Unit, Basic and Applied Medical Sciences, Ghent University, Ghent, Belgium
Interests: hepatology; gastroenterology; inflammation; macrophages; innate immunity; metabolism

Special Issue Information

Dear Colleagues,

We are delighted to invite you to contribute to a Special Issue of Cells, titled “The Gut–Liver Crosstalk in Liver Disease”. The liver and the gut are anatomically united by the portal and enterohepatic circulation, and are functionally allied as the gut–liver axis. The gut and its microbiome have an essential task in the metabolization and absorption of nutrients, which are drained towards the liver via the portal circulation. The liver further metabolizes gut-derived products and produces bile acids, essential for lipid metabolism. In addition to their metabolic interconnection, the gut and the liver are anatomically and functionally organized as barrier tissues. They provide a first and second line of defence against toxins and pathogens, whilst regulating immune tolerance against dietary and microbial antigens in homeostatic conditions. Any harmful substance that passes the intestinal barrier can reach the liver and activate an immune response. Indeed, an intact intestinal barrier is essential for liver homeostasis and increased intestinal permeability, denoted as a “leaky gut”, and consequent bacterial translocation are key factors in the pathogenesis of chronic liver disease. An understanding of the necessity of the intact gut–liver axis for homeostasis has opened the field of research towards uncovering the functional, metabolic, and cellular and molecular mechanisms involved in the maintenance of this gut–liver symbiosis and its disruption during disease. This Special Issue of Cells will specifically focus on the link between the disturbed gut–liver crosstalk and immune dysregulation in liver disease.

We are looking forward to your contributions to this Special Issue.

Prof. Dr. Lindsey Devisscher
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. 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–liver crosstalk
  • Gastro-intestinal-related liver disease
  • Immune dysfunction
  • Chronic liver disease
  • Bacterial translocation
  • Leaky gut

Published Papers (3 papers)

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Research

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20 pages, 3929 KiB  
Article
Systematic Characterization of the Disruption of Intestine during Liver Tumor Progression in the xmrk Oncogene Transgenic Zebrafish Model
by Yan Li, Ai Qi Lee, Zhiyuan Lu, Yuxi Sun, Jeng-Wei Lu, Ziheng Ren, Na Zhang, Dong Liu and Zhiyuan Gong
Cells 2022, 11(11), 1810; https://doi.org/10.3390/cells11111810 - 31 May 2022
Viewed by 2365
Abstract
The crosstalk between tumors and their local microenvironment has been well studied, whereas the effect of tumors on distant tissues remains understudied. Studying how tumors affect other tissues is important for understanding the systemic effect of tumors and for improving the overall health [...] Read more.
The crosstalk between tumors and their local microenvironment has been well studied, whereas the effect of tumors on distant tissues remains understudied. Studying how tumors affect other tissues is important for understanding the systemic effect of tumors and for improving the overall health of cancer patients. In this study, we focused on the changes in the intestine during liver tumor progression, using a previously established liver tumor model through inducible expression of the oncogene xmrk in zebrafish. Progressive disruption of intestinal structure was found in the tumor fish, displaying villus damage, thinning of bowel wall, increase in goblet cell number, decrease in goblet cell size and infiltration of eosinophils, most of which were observed phenotypes of an inflammatory intestine. Intestinal epithelial cell renewal was also disrupted, with decreased cell proliferation and increased cell death. Analysis of intestinal gene expression through RNA-seq suggested deregulation of genes related to intestinal function, epithelial barrier and homeostasis and activation of pathways in inflammation, epithelial mesenchymal transition, extracellular matrix organization, as well as hemostasis. Gene set enrichment analysis showed common gene signatures between the intestine of liver tumor fish and human inflammatory bowel disease, the association of which with cancer has been recently noticed. Overall, this study represented the first systematic characterization of the disruption of intestine under the liver tumor condition and suggested targeting intestinal inflammation as a potential approach for managing cancer cachexia. Full article
(This article belongs to the Special Issue The Gut-Liver Crosstalk in Liver Disease)
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14 pages, 3567 KiB  
Article
Effect of a High-Fat Diet on the Small-Intestinal Environment and Mucosal Integrity in the Gut-Liver Axis
by Takashi Nakanishi, Hirokazu Fukui, Xuan Wang, Shin Nishiumi, Haruka Yokota, Yutaka Makizaki, Yoshiki Tanaka, Hiroshi Ohno, Toshihiko Tomita, Tadayuki Oshima and Hiroto Miwa
Cells 2021, 10(11), 3168; https://doi.org/10.3390/cells10113168 - 14 Nov 2021
Cited by 23 | Viewed by 3109
Abstract
Although high-fat diet (HFD)-related dysbiosis is involved in the development of steatohepatitis, its pathophysiology especially in the small intestine remains unclear. We comprehensively investigated not only the liver pathology but also the microbiome profile, mucosal integrity and luminal environment in the small intestine [...] Read more.
Although high-fat diet (HFD)-related dysbiosis is involved in the development of steatohepatitis, its pathophysiology especially in the small intestine remains unclear. We comprehensively investigated not only the liver pathology but also the microbiome profile, mucosal integrity and luminal environment in the small intestine of mice with HFD-induced obesity. C57BL/6J mice were fed either a normal diet or an HFD, and their small-intestinal contents were subjected to microbial 16S rDNA analysis. Intestinal mucosal permeability was evaluated by FITC-dextran assay. The levels of bile acids in the small-intestinal contents were measured by liquid chromatography/mass spectrometry. The expression of tight junction molecules, antimicrobial peptides, lipopolysaccharide and macrophage marker F4/80 in the small intestine and/or liver was examined by real-time RT-PCR and immunohistochemistry. The abundance of Lactobacillus was markedly increased and that of Clostridium was drastically decreased in the small intestine of mice fed the HFD. The level of conjugated taurocholic acid was significantly increased and those of deconjugated cholic acid/secondary bile acids were conversely decreased in the small-intestinal contents. The expression of occludin, antimicrobial Reg IIIβ/γ and IL-22 was significantly decreased in the small intestine of HFD-fed mice, and the intestinal permeability was significantly accelerated. Infiltration of lipopolysaccharide was significantly increased in not only the small-intestinal mucosa but also the liver of HFD-fed mice, and fat drops were apparently accumulated in the liver. Pathophysiological alteration of the luminal environment in the small intestine resulting from a HFD is closely associated with minimal inflammation involving the gut-liver axis through disturbance of small-intestinal mucosal integrity. Full article
(This article belongs to the Special Issue The Gut-Liver Crosstalk in Liver Disease)
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Review

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34 pages, 1587 KiB  
Review
The Gut–Liver Axis in Chronic Liver Disease: A Macrophage Perspective
by Kevin De Muynck, Bart Vanderborght, Hans Van Vlierberghe and Lindsey Devisscher
Cells 2021, 10(11), 2959; https://doi.org/10.3390/cells10112959 - 30 Oct 2021
Cited by 18 | Viewed by 4849
Abstract
Chronic liver disease (CLD) is a growing health concern which accounts for two million deaths per year. Obesity, alcohol overconsumption, and progressive cholestasis are commonly characterized by persistent low-grade inflammation and advancing fibrosis, which form the basis for development of end-stage liver disease [...] Read more.
Chronic liver disease (CLD) is a growing health concern which accounts for two million deaths per year. Obesity, alcohol overconsumption, and progressive cholestasis are commonly characterized by persistent low-grade inflammation and advancing fibrosis, which form the basis for development of end-stage liver disease complications, including hepatocellular carcinoma. CLD pathophysiology extends to the intestinal tract and is characterized by intestinal dysbiosis, bile acid dysregulation, and gut barrier disruption. In addition, macrophages are key players in CLD progression and intestinal barrier breakdown. Emerging studies are unveiling macrophage heterogeneity and driving factors of their plasticity in health and disease. To date, in-depth investigation of how gut–liver axis disruption impacts the hepatic and intestinal macrophage pool in CLD pathogenesis is scarce. In this review, we give an overview of the role of intestinal and hepatic macrophages in homeostasis and gut–liver axis disruption in progressive stages of CLD. Full article
(This article belongs to the Special Issue The Gut-Liver Crosstalk in Liver Disease)
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