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Special Issue "Update on Basic and Molecular Research in Inflammatory Bowel Disease"

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: 15 January 2020.

Special Issue Editors

Dr. Alfredo Papa
E-Mail Website
Guest Editor
Fondazione Policlinico Gemelli, IRCCS,Catholic University of Rome, Area Medicina Interna, Gastroenterologia ed Oncologia Medica, 00168 Rome, Italy
Interests: Colorectal cancer and dysplasia in inflammatory bowel disease; Helicobacter pylori and gastric cancer; Intestinal lymphoma
Dr. Loris Riccardo Lopetuso
E-Mail
Guest Editor
Internal Medicine and Gastroenterology Department, IRCCS Fondazione Policlinico Gemelli, Catholic University of Rome, 00168 Rome, Italy
Interests: Inflammatory bowel disease (IBD), Target therapy, mucosal immunology, inflammatory cytokines, gut microbiota, intestinal mucosal healing, IBD murine models, tumorigenesis associated to chronic inflammation

Special Issue Information

Dear colleagues,

In the recent years, many advances in the pathogenesis of inflammatory bowel disease (IBD), including Ulcerative colitis and Crohn’s disease, have emerged with a substantial impact on daily clinical practice. These new findings allowed the introduction of new molecular markers and innovative drugs useful for an innovative clinical approach to IBD. We propose to your attention a special issue of IJMS including Reviews and Research Articles regarding recent advances in the field of basic and molecular research with translational applications in IBD.


The establishment of new goals in the management of IBD and the continuation in the understanding of the IBD pathogenic mechanisms have introduced new concepts in the area of intestinal fibrogenesis, small oral therapeutic molecules, gut microbiota, molecular markers of intestinal healing, molecular predictive markers of response to therapy.

In this Special Issue, we will welcome your contributions in the form of original research and review articles facing each side of basic and molecular research in IBD.

Dr. Alfredo Papa
Dr. Loris Riccardo Lopetuso
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 papers will be 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

  • IBD molecular pathogenesis
  • Intestinal mucosal healing
  • Gut microbiota in IBD
  • Faecal microbiota transplantation
  • Target therapy in IBD
  • Stem cells therapy
  • Biologic agents
  • Small molecules
  • Adhesion antagonists
  • Inflammatory cytokines
  • Lymphocyte control

Published Papers (4 papers)

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Research

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Open AccessArticle
Oversecretion and Overexpression of Nicotinamide Phosphoribosyltransferase/Pre-B Colony-Enhancing Factor/Visfatin in Inflammatory Bowel Disease Reflects the Disease Activity, Severity of Inflammatory Response and Hypoxia
Int. J. Mol. Sci. 2019, 20(1), 166; https://doi.org/10.3390/ijms20010166 - 04 Jan 2019
Cited by 1
Abstract
Nicotinamide phosphoribosyltransferase’s (Nampt) association with inflammatory bowel disease (IBD) is unclear. The study was aimed at unraveling Nampt’s clinical and diagnostic relevance. The serum concentration (Luminex-xMAP® technology) was measured in 113 patients with Crohn’s disease (CD), 127 with ulcerative colitis (UC) and 60 [...] Read more.
Nicotinamide phosphoribosyltransferase’s (Nampt) association with inflammatory bowel disease (IBD) is unclear. The study was aimed at unraveling Nampt’s clinical and diagnostic relevance. The serum concentration (Luminex-xMAP® technology) was measured in 113 patients with Crohn’s disease (CD), 127 with ulcerative colitis (UC) and 60 non-IBD controls: 40 healthy individuals and 20 with irritable bowel syndrome (IBS). The leukocyte (44 CD/37 UC/19 IBS) and bowel expression (186 samples) was also evaluated (RT-qPCR). All were referred to IBD phenotype, activity, treatment, and inflammatory/nutritional/angiogenic/hypoxia indices. Serum-Nampt and leukocyte-Nampt were positively correlated and were more elevated in active-IBD than in IBS, with leukocyte-Nampt being a fair differential marker. Serum-Nampt in UC positively correlated with its clinical and endoscopic activity as well as with pro-inflammatory cytokines. Serum-Nampt ≤1.54 ng/mL was a good indicator of mucosal healing. The expression of Nampt was up-regulated both in inflamed and quiescent colon and reflected, similarly to leukocyte-Nampt, the clinical activity of IBD. Bowel-Nampt was independently associated with IL1B and hypoxia-inducible factor 1α (HIF1A) expression in inflamed bowel but with FGF2 expression in quiescent bowel. In summary, Nampt’s elevation in IBD at local and systemic levels, and protein and mRNA levels, reflects IBD activity and is associated with inflammation, hypoxia (active) and tissue repair (inactive disease). Full article
(This article belongs to the Special Issue Update on Basic and Molecular Research in Inflammatory Bowel Disease)
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Open AccessArticle
C-C Motif Ligand 20 (CCL20) and C-C Motif Chemokine Receptor 6 (CCR6) in Human Peripheral Blood Mononuclear Cells: Dysregulated in Ulcerative Colitis and a Potential Role for CCL20 in IL-1β Release
Int. J. Mol. Sci. 2018, 19(10), 3257; https://doi.org/10.3390/ijms19103257 - 20 Oct 2018
Abstract
The chemokine C-C motif ligand 20 (CCL20) is increased in the colonic mucosa during active inflammatory bowel disease (IBD) and can be found both in the epithelium and immune cells in the lamina propria. The present study investigated CCL20 and C-C motif Chemokine [...] Read more.
The chemokine C-C motif ligand 20 (CCL20) is increased in the colonic mucosa during active inflammatory bowel disease (IBD) and can be found both in the epithelium and immune cells in the lamina propria. The present study investigated CCL20 and C-C motif Chemokine Receptor 6 (CCR6) in peripheral blood mononuclear cells (PBMCs) (n = 40) from IBD patients and healthy controls, to identify inductors of CCL20 release encountered in a local proinflammatory environment. CCL20 release from PBMCs was increased when activating TLR2/1 or NOD2, suggesting that CCL20 is part of a first line response to danger-associated molecular patterns also in immune cells. Overall, ulcerative colitis (UC) had a significantly stronger CCL20 release than Crohn’s disease (CD) (+242%, p < 0.01), indicating that the CCL20-CCR6 axis may be more involved in UC. The CCL20 receptor CCR6 is essential for the chemotactic function of CCL20. UC with active inflammation had significantly decreased CCR6 expression and a reduction in CCR6+ cells in circulation, indicating chemoattraction of CCR6+ cells from circulation towards peripheral tissues. We further examined CCL20 induced release of cytokines from PBMCs. Stimulation with CCL20 combined with TNF increased IL-1β release from PBMCs. By attracting additional immune cells, as well as inducing proinflammatory IL-1β release from immune cells, CCL20 may protract the inflammatory response in ulcerative colitis. Full article
(This article belongs to the Special Issue Update on Basic and Molecular Research in Inflammatory Bowel Disease)
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Open AccessArticle
Microparticles Produced by Activated Platelets Carry a Potent and Functionally Active Angiogenic Signal in Subjects with Crohn’s Disease
Int. J. Mol. Sci. 2018, 19(10), 2921; https://doi.org/10.3390/ijms19102921 - 26 Sep 2018
Cited by 3
Abstract
Microparticles (MPs) are submicron vesicles shed from various cell types upon activation, stimulation, and death. Activated platelets are an important source of circulating MPs in subjects with inflammatory diseases, including Crohn’s disease (CD). Angiogenesis is a hallmark of inflammation in CD and plays [...] Read more.
Microparticles (MPs) are submicron vesicles shed from various cell types upon activation, stimulation, and death. Activated platelets are an important source of circulating MPs in subjects with inflammatory diseases, including Crohn’s disease (CD). Angiogenesis is a hallmark of inflammation in CD and plays an active role in sustaining disease progression, while targeting angiogenesis may be an effective approach to block colitis. In this study, we analyzed the angiogenic content of the MPs produced by activated platelets in subjects with CD. We also evaluated whether the angiogenic signal carried by these MPs was functionally active, or able to induce angiogenesis. We found that, in subjects with CD, MPs produced by activated platelets contain significantly higher levels of angiogenic mRNAs, such as epidermal growth factor (EGF), platelet-derived growth factor-α (PDGFα), fibroblast growth factor (FGF-2), and angiopoietin-1 (ANGPT1), compared to MPs isolated from control subjects. They also contain significantly higher levels of prototypical angiogenic proteins, including vascular endothelial growth factor (VEGF), angiopoietin-1, endoglin, endothelin-1, pentraxin 3, platelet factor-4, plasminogen activator inhibitor-1 (PAI-1), tissue inhibitor of metalloproteinases-1 (TIMP-1), and thrombospondin 1. The protein content of these MPs is functionally active, since it has the ability to induce a robust angiogenic process in an endothelial cell/interstitial cell co-culture in vitro assay. Our results reveal a potential novel mechanism through which the angiogenic signal is delivered in subjects with CD, with potentially important clinical and therapeutic implications. Full article
(This article belongs to the Special Issue Update on Basic and Molecular Research in Inflammatory Bowel Disease)
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Review

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Open AccessReview
Omega Fatty Acids and Inflammatory Bowel Diseases: An Overview
Int. J. Mol. Sci. 2019, 20(19), 4851; https://doi.org/10.3390/ijms20194851 - 30 Sep 2019
Abstract
Inflammatory bowel diseases (IBD) are chronic, inflammatory processes that affect the gastrointestinal tract and are mainly represented by ulcerative colitis (UC) and Crohn’s disease (CD). Omega 3 (ω3) fatty acids (eicosapentanoic acid and docosahexaenoic acid) show an indispensable role in the inflammatory processes [...] Read more.
Inflammatory bowel diseases (IBD) are chronic, inflammatory processes that affect the gastrointestinal tract and are mainly represented by ulcerative colitis (UC) and Crohn’s disease (CD). Omega 3 (ω3) fatty acids (eicosapentanoic acid and docosahexaenoic acid) show an indispensable role in the inflammatory processes and, for these reasons, we aimed to review the effects of these acids on UC and CD. Databases such as PUMED and EMBASE were searched, and the final selection included fifteen studies that fulfilled the inclusion criteria. The results showed that ω3 fatty acids reduce intestinal inflammation, induce and maintain clinical remission in UC patients, and are related with the reduction of proinflammatory cytokines, decrease disease activity and increase the quality of life of CD patients. Furthermore, the consumption of these fatty acids may be related to a reduced risk of developing IBD. Many studies have shown the beneficial effects of ω3 as adjunctive in the treatment or prevention of UC or CD. Nevertheless, most were performed with a small number of patients and there are many variations in the mode of consumption, the type of food or the type of formulation used. All these factors substantially interfere with the results and do not allow reliable comparisons. Full article
(This article belongs to the Special Issue Update on Basic and Molecular Research in Inflammatory Bowel Disease)
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