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Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition

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

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 10571

Special Issue Editor

Dr. Susanne M. Krug

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Guest Editor
Institute of Clinical Physiology/Nutritional Medicine, Charité–Universitätsmedizin Berlin, Berlin, Germany
Interests: tricellulin: function, regulation, structure, and clinical impact; the interplay of the impaired tight junction and the subjacent immune cells in inflammation; the role of the tricellular tight junction in inflammatory bowel diseases; inflammatory bowel diseases: barrier defect via IL-13 and tricellulin; tricellular tight junction as a pathway for macromolecules; drug absorption enhancement by targeting the tricellular TJ; neuropathic pain resolution by nerve barrier sealing and netrin-1
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory bowel disease (IBD) is an umbrella term describing chronic idiopathic relapsing and remitting gastrointestinal autoimmune diseases. The main disorders are ulcerative colitis and Crohn’s disease.

IBD has proven to be multifactorial as genetic factors in parallel with environmental, infectious, and immunologic factors have been identified. Dysregulation of transcellular and paracellular intestinal barriers as well as activation of mucosal immune responses are involved either by representing a consequence or a trigger of the pathological impairments.

Recent advances in IBD research have allowed the identification of new molecular predictive markers and development of innovative therapeutic concepts. Nevertheless, the etiological background of IBD remains poorly understood, and basic research with translational applications is cogently needed.

As Volume 1 of the Special Issue “Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases” was successful, we reopen this issue again in the International Journal of Molecular Sciences (ISSN 1422-0067, IF 5.6, JCR Category Q1). This Special Issue aims to gather knowledge of original research and review articles covering functional, ultrastructural, genetic, and molecular research to promote solving the complex puzzle of IBD with the goal on new targets for effective intervention.

Dr. Susanne M. Krug
Guest Editor

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Keywords

  • pathogenesis of inflammatory bowel diseases (IBD)
  • intestinal mucosal inflammation and healing
  • epithelial barrier impairment and regulation
  • mucosal immune cells
  • cytokines and other molecules involved in IBD
  • gut microbiota in IBD
  • therapeutic developments in IBD

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Published Papers (5 papers)

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Research

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16 pages, 1688 KiB  
Article
Perivascular Adipose Tissue Becomes Pro-Contractile and Remodels in an IL10−/− Colitis Model of Inflammatory Bowel Disease
by Samuel W. Jenkins III, Elizabeth A. Grunz, Kassandra R. Ramos and Erika M. Boerman
Int. J. Mol. Sci. 2024, 25(19), 10726; https://doi.org/10.3390/ijms251910726 - 5 Oct 2024
Viewed by 715
Abstract
Inflammatory Bowel Diseases (IBDs) are associated with aberrant immune function, widespread inflammation, and altered intestinal blood flow. Perivascular adipose tissue (PVAT) surrounding the mesenteric vasculature can modulate vascular function and control the local immune cell population, but its structure and function have never [...] Read more.
Inflammatory Bowel Diseases (IBDs) are associated with aberrant immune function, widespread inflammation, and altered intestinal blood flow. Perivascular adipose tissue (PVAT) surrounding the mesenteric vasculature can modulate vascular function and control the local immune cell population, but its structure and function have never been investigated in IBD. We used an IL10−/− mouse model of colitis that shares features with human IBD to test the hypothesis that IBD is associated with (1) impaired ability of PVAT to dilate mesenteric arteries and (2) changes in PVAT resident adipocyte and immune cell populations. Pressure myography and electrical field stimulation of isolated mesenteric arteries show that PVAT not only loses its anti-contractile effect but becomes pro-contractile in IBD. Quantitative immunohistochemistry and confocal imaging studies found significant adipocyte hyperplasia and increased PVAT leukocytes, particularly macrophages, in IBD. PCR arrays suggest that these changes occur alongside the altered cytokine and chemokine gene expression associated with altered NF-κB signaling. Collectively, these results show that the accumulation of macrophages in PVAT during IBD pathogenesis may lead to local inflammation, which ultimately contributes to increased arterial constriction and decreased intestinal blood flow with IBD. Full article
(This article belongs to the Special Issue Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition)
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17 pages, 480 KiB  
Article
Genotype Prevalence of Lactose Deficiency, Vitamin D Deficiency, and the Vitamin D Receptor in a Chilean Inflammatory Bowel Disease Cohort: Insights from an Observational Study
by Tamara Pérez-Jeldres, M. Leonor Bustamante, Roberto Segovia-Melero, Nataly Aguilar, Fabien Magne, Gabriel Ascui, Denisse Uribe, Lorena Azócar, Cristián Hernández-Rocha, Ricardo Estela, Verónica Silva, Andrés De La Vega, Elizabeth Arriagada, Mauricio Gonzalez, Gian-Franco Onetto, Sergio Escobar, Pablo Baez, Alejandra Zazueta, Carolina Pavez-Ovalle, Juan Francisco Miquel and Manuel Álvarez-Lobosadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(19), 14866; https://doi.org/10.3390/ijms241914866 - 3 Oct 2023
Cited by 1 | Viewed by 2029
Abstract
Lactose intolerance (LI) and vitamin D deficiency (VDD) have been linked to inflammatory bowel disease (IBD). We conducted an observational study in 192 Chilean IBD patients to investigate the prevalence of a specific gene variant (LCT-13910 CC genotype) associated with LI and the [...] Read more.
Lactose intolerance (LI) and vitamin D deficiency (VDD) have been linked to inflammatory bowel disease (IBD). We conducted an observational study in 192 Chilean IBD patients to investigate the prevalence of a specific gene variant (LCT-13910 CC genotype) associated with LI and the prevalence of VDD/Vitamin D Receptor (VDR) gene variants. Blood samples were analyzed using Illumina’s Infinium Global Screening Array. The LCT-13910 CC genotype was found in 61% of IBD patients, similar to Chilean Hispanic controls and lower than Chilean Amerindian controls. The frequency of the LCT-13910-C allele in Chilean IBD patients (0.79) was comparable to the general population and higher than Europeans (0.49). Regarding VDR and VDD variants, in our study, the rs12785878-GG variant was associated with an increased risk of IBD (OR = 2.64, CI = 1.61–4.32; p-value = 0.001). Sixty-one percent of the Chilean IBD cohort have a genetic predisposition to lactose malabsorption, and a significant proportion exhibit genetic variants associated with VDD/VDR. Screening for LI and VDD is crucial in this Latin American IBD population. Full article
(This article belongs to the Special Issue Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition)
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Review

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23 pages, 3322 KiB  
Review
Eosinophilic Esophagitis and Inflammatory Bowel Disease: What Are the Differences?
by Hassan Melhem and Jan Hendrik Niess
Int. J. Mol. Sci. 2024, 25(15), 8534; https://doi.org/10.3390/ijms25158534 - 5 Aug 2024
Viewed by 1335
Abstract
Eosinophilic esophagitis (EoE) and inflammatory bowel disease (IBD) are chronic inflammatory disorders of the gastrointestinal tract, with EoE predominantly provoked by food and aeroallergens, whereas IBD is driven by a broader spectrum of immunopathological and environmental triggers. This review presents a comprehensive comparison [...] Read more.
Eosinophilic esophagitis (EoE) and inflammatory bowel disease (IBD) are chronic inflammatory disorders of the gastrointestinal tract, with EoE predominantly provoked by food and aeroallergens, whereas IBD is driven by a broader spectrum of immunopathological and environmental triggers. This review presents a comprehensive comparison of the pathophysiological and therapeutic strategies for EoE and IBD. We examine the current understanding of their underlying mechanisms, particularly the interplay between environmental factors and genetic susceptibility. A crucial element in both diseases is the integrity of the epithelial barrier, whose disruption plays a central role in their pathogenesis. The involvement of eosinophils, mast cells, B cells, T cells, dendritic cells, macrophages, and their associated cytokines is examined, highlighting the importance of targeting cytokine signaling pathways to modulate immune–epithelial interactions. We propose that advances in computation tools will uncover the significance of G-protein coupled receptors (GPCRs) in connecting immune and epithelial cells, leading to novel therapies for EoE and IBD. Full article
(This article belongs to the Special Issue Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition)
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34 pages, 1690 KiB  
Review
Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease
by Barbara Sosna, David Aebisher, Angelika Myśliwiec, Klaudia Dynarowicz, Dorota Bartusik-Aebisher, Piotr Oleś, Grzegorz Cieślar and Aleksandra Kawczyk-Krupka
Int. J. Mol. Sci. 2024, 25(1), 202; https://doi.org/10.3390/ijms25010202 - 22 Dec 2023
Cited by 2 | Viewed by 1897
Abstract
Inflammatory bowel disease (IBD) is a collective term for two diseases: ulcerative colitis (UC) and Crohn’s disease (CD). There are many factors, e.g., genetic, environmental and immunological, that increase the likelihood of these diseases. Indicators of IBDs include extracellular matrix metalloproteinases (MMPs). The [...] Read more.
Inflammatory bowel disease (IBD) is a collective term for two diseases: ulcerative colitis (UC) and Crohn’s disease (CD). There are many factors, e.g., genetic, environmental and immunological, that increase the likelihood of these diseases. Indicators of IBDs include extracellular matrix metalloproteinases (MMPs). The aim of this review is to present data on the role of selected cytokines and metalloproteinases in IBD. In recent years, more and more transcriptomic studies are emerging. These studies are improving the characterization of the cytokine microenvironment inside inflamed tissue. It is observed that the levels of several cytokines are consistently increased in inflamed tissue in IBD, both in UC and CD. This review shows that MMPs play a major role in the pathology of inflammatory processes, cancer, and IBD. IBD-associated inflammation is associated with increased expression of MMPs and reduced ability of tissue inhibitors of metalloproteinases (TIMPs) to inhibit their action. In IBD patients in tissues that are inflamed, MMPs are produced in excess and TIMP activity is not sufficient to block MMPs. This review is based on our personal selection of the literature that was retrieved by a selective search in PubMed using the terms “Inflammatory bowel disease” and “pathogenesis of Inflammatory bowel diseases” that includes systematic reviews, meta-analyses, and clinical trials. The involvement of the immune system in the pathophysiology of IBD is reviewed in terms of the role of the cytokines and metalloproteinases involved. Full article
(This article belongs to the Special Issue Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition)
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33 pages, 3544 KiB  
Review
Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review
by María José Sánchez-Quintero, Cristina Rodríguez-Díaz, Francisco J. Rodríguez-González, Alejandra Fernández-Castañer, Eduardo García-Fuentes and Carlos López-Gómez
Int. J. Mol. Sci. 2023, 24(23), 17124; https://doi.org/10.3390/ijms242317124 - 4 Dec 2023
Cited by 4 | Viewed by 3789
Abstract
Mitochondria are key cellular organelles whose main function is maintaining cell bioenergetics by producing ATP through oxidative phosphorylation. However, mitochondria are involved in a much higher number of cellular processes. Mitochondria are the home of key metabolic pathways like the tricarboxylic acid cycle [...] Read more.
Mitochondria are key cellular organelles whose main function is maintaining cell bioenergetics by producing ATP through oxidative phosphorylation. However, mitochondria are involved in a much higher number of cellular processes. Mitochondria are the home of key metabolic pathways like the tricarboxylic acid cycle and β-oxidation of fatty acids, as well as biosynthetic pathways of key products like nucleotides and amino acids, the control of the redox balance of the cell and detoxifying the cell from H2S and NH3. This plethora of critical functions within the cell is the reason mitochondrial function is involved in several complex disorders (apart from pure mitochondrial disorders), among them inflammatory bowel diseases (IBD). IBD are a group of chronic, inflammatory disorders of the gut, mainly composed of ulcerative colitis and Crohn’s disease. In this review, we present the current knowledge regarding the impact of mitochondrial dysfunction in the context of IBD. The role of mitochondria in both intestinal mucosa and immune cell populations are discussed, as well as the role of mitochondrial function in mechanisms like mucosal repair, the microbiota– and brain–gut axes and the development of colitis-associated colorectal cancer. Full article
(This article belongs to the Special Issue Solving the Puzzle: Molecular Research in Inflammatory Bowel Diseases, 2nd Edition)
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