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Gut and the Liver in Health and Disease 2.0

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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 (31 October 2023) | Viewed by 17363

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Dr. Pavel Strnad

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Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany
Interests: internal medicine; liver diseases; liver cirrhosis; gastroenterology; chronic hepatitis C
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Special Issue Information

Dear Colleagues,

The gut and the liver build a functional unit responsible for the digestion and processing of nutrients. The crosstalk between both organs is achieved by an exchange of factors. It is facilitated by a joint vascular system as well as by the hepatobiliary circulation of the bile and its constituents. The current Special Issue of IJMS aims to reflect the physiology and pathophysiology of both organs with a particular focus on the role of microbiota, bile acids, and soluble factors circulating in the blood. The submission of manuscripts providing insights into the corresponding human disorders is strongly encouraged, regardless of whether they stem from analyses of human samples or from experimental animal models. Both acute and chronic injury with processes such as hepatocellular death, the influx of inflammatory cells, and chronic tissue remodeling are of interest, as is the analysis of affected signaling pathways. Advanced liver fibrosis with the development of portal hypertension and associated alterations of the gut–liver unit are mostly welcome. Overall, this Special Issue aims to reflect the complexity of this functional unit and bring together biologists, immunologists, physician scientists, and bioinformaticians.

We invite authors to submit original research and review articles regarding the molecular/clinical aspects, including but not limited to the following topics:

Chronic intestinal disorders such as celiac disease or inflammatory bowel disease;
Acute and chronic liver injury;
Animal models of human disease;
Gut–liver axis;
Signaling;
Liver cirrhosis and its complications;
Intestinal microbiota.

Dr. Pavel Strnad
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.

Published Papers (12 papers)

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Research

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21 pages, 4748 KiB

Open AccessArticle

The Ameliorating Effects of n-3 Polyunsaturated Fatty Acids on Liver Steatosis Induced by a High-Fat Methionine Choline-Deficient Diet in Mice

by Václav Šmíd, Karel Dvořák, Kamila Stehnová, Hynek Strnad, Josep Rubert, Jan Stříteský, Barbora Staňková, Milena Stránská, Jana Hajšlová, Radan Brůha and Libor Vítek

Int. J. Mol. Sci. 2023, 24(24), 17226; https://doi.org/10.3390/ijms242417226 - 07 Dec 2023

Viewed by 1013

Abstract

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is associated with abnormalities of liver lipid metabolism. On the contrary, a diet enriched with n-3 polyunsaturated fatty acids (n-3-PUFAs) has been reported to ameliorate the progression of NAFLD. The aim of our study was to investigate the impact of dietary n-3-PUFA enrichment on the development of NAFLD and liver lipidome. Mice were fed for 6 weeks either a high-fat methionine choline-deficient diet (MCD) or standard chow with or without n-3-PUFAs. Liver histology, serum biochemistry, detailed plasma and liver lipidomic analyses, and genome-wide transcriptome analysis were performed. Mice fed an MCD developed histopathological changes characteristic of NAFLD, and these changes were ameliorated with n-3-PUFAs. Simultaneously, n-3-PUFAs decreased serum triacylglycerol and cholesterol concentrations as well as ALT and AST activities. N-3-PUFAs decreased serum concentrations of saturated and monounsaturated free fatty acids (FAs), while increasing serum concentrations of long-chain PUFAs. Furthermore, in the liver, the MCD significantly increased the hepatic triacylglycerol content, while the administration of n-3-PUFAs eliminated this effect. Administration of n-3-PUFAs led to significant beneficial differences in gene expression within biosynthetic pathways of cholesterol, FAs, and pro-inflammatory cytokines (IL-1 and TNF-α). To conclude, n-3-PUFA supplementation appears to represent a promising nutraceutical approach for the restoration of abnormalities in liver lipid metabolism and the prevention and treatment of NAFLD. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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14 pages, 7534 KiB

Open AccessArticle

Inactivation of Group 1B Phospholipase A₂ Enhances Disease Recovery and Reduces Experimental Colitis in Mice

by April M. Haller, Patrick R. Wolfkiel, Anja Jaeschke and David Y. Hui

Int. J. Mol. Sci. 2023, 24(22), 16155; https://doi.org/10.3390/ijms242216155 - 10 Nov 2023

Viewed by 908

Abstract

Phospholipase A₂ (PLA₂) enzymes influence inflammatory bowel disease in both positive and negative manners depending on the type of PLA₂ that is expressed. This study explored the influence of the abundantly expressed Group 1B PLA₂ (PLA2G1B) on ulcerative colitis. Wild-type C57BL/6J mice and Pla2g1b^−/− mice were treated with dextran sulfate sodium (DSS) for 5 days to induce epithelial injury, followed by another 5 days without DSS for recovery. The Pla2g1b^−/− mice displayed significantly less body weight loss, colitis pathology, and disease activity indexes compared to the wild-type mice. The differences in colitis were not due to differences in the colonic lysophospholipid levels, but higher numbers of stem and progenitor cells were found in the intestines of Pla2g1b^−/− mice compared to the wild-type mice. The DSS-treated Pla2g1b^−/− mice also showed higher expressions of genes that are responsible for epithelial repair and lower expressions of proinflammatory cytokine genes in the colon, as well as reduced inflammatory cytokine levels in the plasma. In vitro experiments revealed the PLA2G1B stimulation of inflammatory cytokine expression by myeloid cells. PLA2G1B inactivation protects against DSS-induced colitis in mice by increasing the intestinal stem cell reservoir for epithelial repair and reducing myeloid cell inflammation in the diseased colon. Thus, PLA2G1B may be a target for colitis management. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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14 pages, 1763 KiB

Open AccessArticle

Elevated Liver Fibrosis Progression in Isolated PSC Patients and Increased Malignancy Risk in a PSC-IBD Cohort: A Retrospective Study

by Florian Rennebaum, Claudia Demmig, Hartmut H. Schmidt, Richard Vollenberg, Phil-Robin Tepasse, Jonel Trebicka, Wenyi Gu, Hansjoerg Ullerich, Iyad Kabar and Friederike Cordes

Int. J. Mol. Sci. 2023, 24(20), 15431; https://doi.org/10.3390/ijms242015431 - 21 Oct 2023

Viewed by 1241

Abstract

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease often associated with inflammatory bowel disease (IBD), particularly ulcerative colitis (CU), and rarely with Crohn’s disease (CD). Various long-term analyses show different rates of cancer and the need for orthotopic liver transplantation (OLT) in patients with isolated PSC and with concomitant IBD, respectively. However, data on the detailed course of PSC with or without IBD are limited. We aimed to analyze the clinical disease course of PSC patients without IBD compared to PSC patients with UC and CD, respectively. A retrospective data analysis of patients with isolated PSC (n = 41) and of patients with concomitant IBD (n = 115) was performed. In detail, PSC disease characteristics including occurrence of dominant stenoses, liver cirrhosis, OLT and malignancy, as well as the temporal course of PSC activity and disease progression, were analyzed. A multivariable Cox regression model and a Fine–Gray competing risk model were further used for the independent risk factor analysis of cirrhosis development and OLT. Patients with isolated PSC were significantly older at first diagnosis than patients with PSC-IBD (39 vs. 28 years, p = 0.02). A detailed analysis of the course of PSC revealed a faster PSC progression after initial diagnosis in isolated PSC patients compared to PSC-IBD including significantly earlier diagnosis of dominant stenoses (29 vs. 74 months, p = 0.021) and faster progression to liver cirrhosis (38 vs. 103 months, p = 0.027). Patients with isolated PSC have a higher risk of developing cirrhosis than patients with PSC-IBD (Gray’s test p = 0.03). OLT was more frequently performed in male patients with isolated PSC compared to males with coincident IBD (48% (n = 13) vs. 33% (n = 25), p = 0.003). Colorectal carcinoma was significantly more often diagnosed in patients with PSC-IBD than in isolated PSC (8.7% vs. 0%, p = 0.042). Patients with isolated PSC seem to have a different clinical course of disease than PSC patients with concomitant IBD characterized by a more pro-fibrotic disease course with earlier onset of liver cirrhosis and dominant stenosis but with less malignancy. These data may be interpreted as either a more progressive disease course of isolated PSC or a later diagnosis of the disease at an advanced disease stage. The different clinical courses of PSC and the underlying mechanisms of the gut–liver axis need further attention. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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15 pages, 5677 KiB

Open AccessArticle

Experimental Liver Cirrhosis Inhibits Restenosis after Balloon Angioplasty

by Mare Mechelinck, Marc Hein, Carolin Kupp, Till Braunschweig, Marius J. Helmedag, Axel Klinkenberg, Moriz A. Habigt, Uwe Klinge, René H. Tolba and Moritz Uhlig

Int. J. Mol. Sci. 2023, 24(14), 11351; https://doi.org/10.3390/ijms241411351 - 12 Jul 2023

Viewed by 1210

Abstract

The effect of liver cirrhosis on vascular remodeling in vivo remains unknown. Therefore, this study investigates the influence of cholestatic liver cirrhosis on carotid arterial remodeling. A total of 79 male Sprague Dawley rats underwent bile duct ligation (cirrhotic group) or sham surgery (control group) and 28 days later left carotid artery balloon dilatation; 3, 7, 14 and 28 days after balloon dilatation, the rats were euthanized and carotid arteries were harvested. Histological sections were planimetrized, cell counts determined, and systemic inflammatory parameters measured. Up to day 14 after balloon dilatation, both groups showed a comparable increase in neointima area and degree of stenosis. By day 28, however, both values were significantly lower in the cirrhotic group (% stenosis: 20 ± 8 vs. 42 ± 10, p = 0.010; neointimal area [mm²]: 0.064 ± 0.025 vs. 0.138 ± 0.025, p = 0.024). Simultaneously, cell density in the neointima (p = 0.034) and inflammatory parameters were significantly higher in cirrhotic rats. This study demonstrates that cholestatic liver cirrhosis in rats substantially increases neointimal cell consolidation between days 14 and 28. Thereby, consolidation proved important for the degree of stenosis. This may suggest that patients with cholestatic cirrhosis are at lower risk for restenosis after coronary intervention. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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10 pages, 2826 KiB

Open AccessCommunication

Hfe Actions in Kupffer Cells Are Dispensable for Hepatic and Systemic Iron Metabolism

by Paul Knoop, Dilay Yilmaz, Rossana Paganoni, Peter Steele-Perkins, Andreas Gruber, Banu Akdogan, Hans Zischka, Kerstin Leopold and Maja Vujić Spasić

Int. J. Mol. Sci. 2023, 24(10), 8948; https://doi.org/10.3390/ijms24108948 - 18 May 2023

Viewed by 1265

Abstract

Mutations in the HFE/Hfe gene cause Hereditary Hemochromatosis (HH), a highly prevalent genetic disorder characterized by elevated iron deposition in multiple tissues. HFE acts in hepatocytes to control hepcidin expression, whereas HFE actions in myeloid cells are required for cell-autonomous and systemic iron regulation in aged mice. To address the role of HFE specifically in liver-resident macrophages, we generated mice with a selective Hfe deficiency in Kupffer cells (Hfe^Clec4fCre). The analysis of the major iron parameters in this novel Hfe^Clec4fCre mouse model led us to the conclusion that HFE actions in Kupffer cells are largely dispensable for cellular, hepatic and systemic iron homeostasis. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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Review

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16 pages, 884 KiB

Open AccessReview

The Complex Relationship between Mechanisms Underlying Inflammatory Bowel Disease, Its Treatment, and the Risk of Lymphomas: A Comprehensive Review

by Katarzyna Stasik and Rafał Filip

Int. J. Mol. Sci. 2024, 25(8), 4241; https://doi.org/10.3390/ijms25084241 - 11 Apr 2024

Viewed by 426

Abstract

Patients with inflammatory bowel disease may be at higher risk of developing lymphomas and other cancers of the gastrointestinal tract. In addition, there may be a link between the use of thiopurines or anti-tumor necrosis factor drugs (anti-TNF) and these pathologies. The treatment of patients with Crohn’s disease who have previously been diagnosed with lymphoma is a challenge for gastroenterologists. In this report, we examine important clinical issues related to the treatment of patients with inflammatory bowel disease with active lymphoma, as well as of patients with hematological cancer history. In this discussion, we take into account most of the available treatments for inflammatory bowel disease, as well as the impact of chronic inflammation and viral infections. In addition, we try to find common ground for the development of lymphoproliferative disorders and autoimmune diseases. Patients with inflammatory bowel disease may be at higher risk of developing lymphomas and other cancers of the gastrointestinal tract. Chronic inflammatory processes and viral infections play an important role in carcinogenesis. In addition, there may be a link between the use of thiopurines or anti-TNF drugs and these pathologies. A significant risk of the development of lymphoma in people undergoing each therapy should be considered, and it should be estimated how much greater this risk will be in patients with a history of lymphoproliferative disorders. The following review is an attempt to answer which therapy would be the most appropriate for patients with Crohn’s disease and a history of lymphoma treatment. A lack of clear guidelines creates great challenges for doctors. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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16 pages, 984 KiB

Open AccessReview

Inflammatory Bowel Diseases and Non-Alcoholic Fatty Liver Disease: Piecing a Complex Puzzle Together

by Rossella Maresca, Irene Mignini, Simone Varca, Valentin Calvez, Fabrizio Termite, Giorgio Esposto, Lucrezia Laterza, Franco Scaldaferri, Maria Elena Ainora, Antonio Gasbarrini and Maria Assunta Zocco

Int. J. Mol. Sci. 2024, 25(6), 3278; https://doi.org/10.3390/ijms25063278 - 14 Mar 2024

Viewed by 776

Abstract

Inflammatory bowel diseases (IBD), comprising Crohn’s disease and ulcerative colitis, are systemic and multifaceted disorders which affect other organs in addition to the gastrointestinal tract in up to 50% of cases. Extraintestinal manifestations may present before or after IBD diagnosis and negatively impact the intestinal disease course and patients’ quality of life, often requiring additional diagnostic evaluations or specific treatments. Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. Current evidence shows an increased prevalence of NAFLD (and its more advanced stages, such as liver fibrosis and steatohepatitis) in IBD patients compared to the general population. Many different IBD-specific etiopathogenetic mechanisms have been hypothesized, including chronic inflammation, malabsorption, previous surgical interventions, changes in fecal microbiota, and drugs. However, the pathophysiological link between these two diseases is still poorly understood. In this review, we aim to provide a comprehensive overview of the potential mechanisms which have been investigated so far and highlight open issues still to be addressed for future studies. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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17 pages, 1203 KiB

Open AccessReview

Serum/Plasma Proteome in Non-Malignant Liver Disease

by Lei Fu, Nurdan Guldiken, Katharina Remih, Anna Sophie Karl, Christian Preisinger and Pavel Strnad

Int. J. Mol. Sci. 2024, 25(4), 2008; https://doi.org/10.3390/ijms25042008 - 07 Feb 2024

Viewed by 1431

Abstract

The liver is the central metabolic organ and produces 85–90% of the proteins found in plasma. Accordingly, the plasma proteome is an attractive source of liver disease biomarkers that reflects the different cell types present in this organ, as well as the processes such as responses to acute and chronic injury or the formation of an extracellular matrix. In the first part, we summarize the biomarkers routinely used in clinical evaluations and their biological relevance in the different stages of non-malignant liver disease. Later, we describe the current proteomic approaches, including mass spectrometry and affinity-based techniques, that allow a more comprehensive assessment of the liver function but also require complex data processing. The many approaches of analysis and interpretation and their potential caveats are delineated. While these advances hold the promise to transform our understanding of liver diseases and support the development and validation of new liver-related drugs, an interdisciplinary collaboration is needed. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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16 pages, 1283 KiB

Open AccessReview

Recent Progress in Systemic Therapy for Advanced Hepatocellular Carcinoma

by Narayanan Sadagopan and Aiwu Ruth He

Int. J. Mol. Sci. 2024, 25(2), 1259; https://doi.org/10.3390/ijms25021259 - 19 Jan 2024

Cited by 1 | Viewed by 1469

Abstract

Patients with advanced hepatocellular carcinoma (HCC) have several systemic treatment options. There are many known risk factors for HCC, and although some, such as hepatitis C, are now treatable, others are not. For example, metabolic dysfunction-related chronic liver disease is increasing in incidence and has no specific treatment. Underlying liver disease, drug resistance, and an increasing number of treatment options without specific biomarkers are all challenges in selecting the best treatment for each patient. Conventional chemotherapy is almost never used for advanced-stage disease, which instead is treated with immunotherapy, tyrosine kinase inhibitors, and VEGF inhibitors. Immune checkpoint inhibitors targeting various receptors have been or are currently undergoing clinical evaluation. Ongoing trials with three-drug regimens may be the future of advanced-stage HCC treatment. Other immune-modulatory approaches of chimeric antigen receptor-modified T cells, bispecific antibodies, cytokine-induced killer cells, natural killer cells, and vaccines are in early-stage clinical trials. Targeted therapies remain limited for HCC but represent an area of potential growth. As we shift away from first-line sorafenib for advanced HCC, clinical trial control arms should comprise a standard treatment other than sorafenib, one that is a better comparator for advancing therapies. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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31 pages, 2492 KiB

Open AccessReview

Gut Microbiota and Mitochondria: Health and Pathophysiological Aspects of Long COVID

by Laura Marinela Ailioaie, Constantin Ailioaie and Gerhard Litscher

Int. J. Mol. Sci. 2023, 24(24), 17198; https://doi.org/10.3390/ijms242417198 - 06 Dec 2023

Viewed by 2516

Abstract

The current understanding of long COVID (LC) is still limited. This review highlights key findings regarding the role of gut microbiota, mitochondria, and the main pathophysiological aspects of LC revealed by clinical studies, related to the complex interplay between infection, intestinal dysbiosis, dysfunctional mitochondria, and systemic inflammation generated in a vicious circle, reflecting the molecular and cellular processes from the “leaky gut” to the “leaky electron transport chain (ETC)” into a quantum leap. The heterogeneity of LC has hindered progress in deciphering all the pathophysiological mechanisms, and therefore, the approach must be multidisciplinary, with a special focus not only on symptomatic management but also on addressing the underlying health problems of the patients. It is imperative to further assess and validate the effects of COVID-19 and LC on the gut microbiome and their relationship to infections with other viral agents or pathogens. Further studies are needed to better understand LC and expand the interdisciplinary points of view that are required to accurately diagnose and effectively treat this heterogeneous condition. Given the ability of SARS-CoV-2 to induce autoimmunity in susceptible patients, they should be monitored for symptoms of autoimmune disease after contracting the viral infection. One question remains open, namely, whether the various vaccines developed to end the pandemic will also induce autoimmunity. Recent data highlighted in this review have revealed that the persistence of SARS-CoV-2 and dysfunctional mitochondria in organs such as the heart and, to a lesser extent, the kidneys, liver, and lymph nodes, long after the organism has been able to clear the virus from the lungs, could be an explanation for LC. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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23 pages, 1965 KiB

Open AccessReview

Current and Novel Therapies for Eosinophilic Gastrointestinal Diseases

by Giovanni Marasco, Pierfrancesco Visaggi, Mariagiulia Vassallo, Miriam Fiocca, Cesare Cremon, Maria Raffaella Barbaro, Nicola De Bortoli, Massimo Bellini, Vincenzo Stanghellini, Edoardo Vincenzo Savarino and Giovanni Barbara

Int. J. Mol. Sci. 2023, 24(20), 15165; https://doi.org/10.3390/ijms242015165 - 13 Oct 2023

Cited by 5 | Viewed by 2297

Abstract

Eosinophilic gastrointestinal diseases (EGIDs) are an emerging group of pathological entities characterized by an eosinophil-predominant infiltration of different tracts of the gut in the absence of secondary causes of eosinophilia. According to the specific tract of the gut involved, EGIDs can be classified into eosinophilic esophagitis (EoE), eosinophilic gastritis (EoG), eosinophilic enteritis (EoN), and eosinophilic colitis (EoC). The epidemiology of EGIDs is evolving rapidly. EoE, once considered a rare disease, now has an incidence and prevalence of 7.7 new cases per 100,000 inhabitants per years and 34.4 cases per 100,000 inhabitants per year, respectively. Fewer data are available regarding non-EoE EGIDs, whose prevalence are estimated to range between 2.1 and 17.6 in 100,000 individuals, depending on age, sex, and ethnicity. Diagnosis requires the presence of suggestive symptoms, endoscopic biopsies showing abnormal values of eosinophils infiltrating the gut, and exclusion of secondary causes of eosinophilia. EoE typically presents with dysphagia and episodes of food bolus impactions, while EoG, EoN, and EoC may all present with abdominal pain and diarrhea, with or without other non-specific symptoms. In addition, although different EGIDs are currently classified as different entities, there may be overlap between different diseases in the same patient. Despite EGIDs being relatively novel pathological entities, the research on possible treatments is rapidly growing. In this regard, several randomized controlled trials are currently ongoing to investigate novel molecules, including ad-hoc steroid formulations, immunosuppressants, and mostly monoclonal antibodies that target the specific molecular mediators of EGIDs. This narrative review provides an up-to-date overview of available and investigational drugs for different EGIDs. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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28 pages, 1560 KiB

Open AccessReview

A Current State of Proteomics in Adult and Pediatric Inflammatory Bowel Diseases: A Systematic Search and Review

by Ondrej Fabian, Lukas Bajer, Pavel Drastich, Karel Harant, Eva Sticova, Nikola Daskova, Istvan Modos, Filip Tichanek and Monika Cahova

Int. J. Mol. Sci. 2023, 24(11), 9386; https://doi.org/10.3390/ijms24119386 - 27 May 2023

Cited by 2 | Viewed by 1859

Abstract

Inflammatory bowel diseases (IBD) are systemic immune-mediated conditions with predilection for the gastrointestinal tract and include Crohn’s disease and ulcerative colitis. Despite the advances in the fields of basic and applied research, the etiopathogenesis remains largely unknown. As a result, only one third of the patients achieve endoscopic remission. A substantial portion of the patients also develop severe clinical complications or neoplasia. The need for novel biomarkers that can enhance diagnostic accuracy, more precisely reflect disease activity, and predict a complicated disease course, thus, remains high. Genomic and transcriptomic studies contributed substantially to our understanding of the immunopathological pathways involved in disease initiation and progression. However, eventual genomic alterations do not necessarily translate into the final clinical picture. Proteomics may represent a missing link between the genome, transcriptome, and phenotypical presentation of the disease. Based on the analysis of a large spectrum of proteins in tissues, it seems to be a promising method for the identification of new biomarkers. This systematic search and review summarize the current state of proteomics in human IBD. It comments on the utility of proteomics in research, describes the basic proteomic techniques, and provides an up-to-date overview of available studies in both adult and pediatric IBD. Full article

(This article belongs to the Special Issue Gut and the Liver in Health and Disease 2.0)

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