Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

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

Special Issue Editors
Special Issue Information
Keywords
Published Papers

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: 30 June 2024 | Viewed by 4651

Share This Special Issue

Special Issue Editor

Dr. Susanne M. Krug

E-Mail
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

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

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

Published Papers (3 papers)

Download All Papers

Research

Jump to: Review

17 pages, 480 KiB

Open AccessArticle

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-Lobos Show full author list Hide full author list

Int. J. Mol. Sci. 2023, 24(19), 14866; https://doi.org/10.3390/ijms241914866 - 03 Oct 2023

Viewed by 1326

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 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)

► Show Figures

Figure 1

Review

Jump to: Research

34 pages, 1690 KiB

Open AccessReview

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

Viewed by 944

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 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)

► Show Figures

Figure 1

33 pages, 3544 KiB

Open AccessReview

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 - 04 Dec 2023

Cited by 1 | Viewed by 1934

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 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)

► Show Figures