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Molecular Research in Inflammatory Bowel Disease 2.0

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 March 2021) | Viewed by 15481

Special Issue Editors

1. Department of Translational Medicine and Surgery, School of Medicine, Catholic University, 00168 Rome, Italy
2. Center for Diagnosis and Treatment of Digestive Diseases, CEMAD, Gastroenterology Department, Fondazione Policlinico Gemelli, IRCCS, 00168 Rome, Italy
Interests: inflammatory bowel disease (IBD); ulcerative colitis; Crohn’s disease; target therapy; biologic agents; small molecules; adhesion antagonists; anti-TNF; IBD vascular complications; stem-cells application in IBD; intestinal mucosal healing; gut microbiota
Special Issues, Collections and Topics in MDPI journals
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 Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

In 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. This Special Issue of IJMS will publish 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 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 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

  • IBD molecular pathogenesis
  • Intestinal mucosal healing
  • Gut microbiota in IBD
  • Fecal 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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17 pages, 3178 KiB  
Article
Anti-Inflammatory Activity of Oat Beta-Glucans in a Crohn’s Disease Model: Time- and Molar Mass-Dependent Effects
by Ewa Żyła, Katarzyna Dziendzikowska, Dariusz Kamola, Jacek Wilczak, Rafał Sapierzyński, Joanna Harasym and Joanna Gromadzka-Ostrowska
Int. J. Mol. Sci. 2021, 22(9), 4485; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094485 - 25 Apr 2021
Cited by 16 | Viewed by 3199
Abstract
Background: The incidence of Crohn’s disease (CD) is increasing worldwide, and it has currently become a serious public health issue in society. The treatment of CD continues throughout a patient’s lifetime, and therefore, it is necessary to develop new, effective treatment methods, including [...] Read more.
Background: The incidence of Crohn’s disease (CD) is increasing worldwide, and it has currently become a serious public health issue in society. The treatment of CD continues throughout a patient’s lifetime, and therefore, it is necessary to develop new, effective treatment methods, including dietotherapy. The present study aimed to determine the effects of consumption of oat beta-glucans with different molar mass on colon inflammation (colitis) in the early stages of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD in an animal model. Methods: Sprague–Dawley rats (control and TNBS-induced CD) were divided into three dietary groups and fed for 3 days (reflecting acute inflammation) or 7 days (reflecting remission) with a feed containing 1% low (βGl) or high (βGh) molar mass oat beta-glucan or a feed without this polysaccharide. The level of colon inflammatory markers and the expression of cytokines and their receptor genes were measured by ELISA and RT-PCR methods, respectively. Results: Acute inflammation or remission (3 or 7 days after TNBS administration, respectively) stages of experimentally induced CD were characterized by an increase in the level of inflammatory markers (IL-1, IL-6, IL-10, IL-12, TNF-α, CRP, MPO, COX, and PGE2) and the disruption of some cytokine signaling pathways as well as macro- and microscopic changes of colon tissue. The consumption of oat beta-glucans reduced the level of inflammatory markers and recovered the signaling pathways and histological changes, with stronger effects of βGl after 7 days of colitis. Conclusions: Dietary oat beta-glucans can reduce colitis at the molecular and organ level and accelerate CD remission. Full article
(This article belongs to the Special Issue Molecular Research in Inflammatory Bowel Disease 2.0)
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19 pages, 4972 KiB  
Article
Extensive Histopathological Characterization of Inflamed Bowel in the Dextran Sulfate Sodium Mouse Model with Emphasis on Clinically Relevant Biomarkers and Targets for Drug Development
by Rita Bonfiglio, Filippo Galli, Michela Varani, Manuel Scimeca, Filippo Borri, Sara Fazi, Rosella Cicconi, Maurizio Mattei, Giuseppe Campagna, Tanja Schönberger, Ernest Raymond, Andreas Wunder, Alberto Signore and Elena Bonanno
Int. J. Mol. Sci. 2021, 22(4), 2028; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042028 - 18 Feb 2021
Cited by 6 | Viewed by 2473
Abstract
This study aims to develop a reliable and reproducible inflammatory bowel disease (IBD) murine model based on a careful spatial–temporal histological characterization. Secondary aims included extensive preclinical studies focused on the in situ expression of clinically relevant biomarkers and targets involved in IBD. [...] Read more.
This study aims to develop a reliable and reproducible inflammatory bowel disease (IBD) murine model based on a careful spatial–temporal histological characterization. Secondary aims included extensive preclinical studies focused on the in situ expression of clinically relevant biomarkers and targets involved in IBD. C57BL/6 female mice were used to establish the IBD model. Colitis was induced by the oral administration of 2% Dextran Sulfate Sodium (DSS) for 5 days, followed by 2, 4 or 9 days of water. Histological analysis was performed by sectioning the whole colon into rings of 5 mm each. Immunohistochemical analyses were performed for molecular targets of interest for monitoring disease activity, treatment response and predicting outcome. Data reported here allowed us to develop an original scoring method useful as a tool for the histological assessment of preclinical models of DSS-induced IBD. Immunohistochemical data showed a significant increase in TNF-α, α4β7, VEGFRII, GR-1, CD25, CD3 and IL-12p40 expression in DSS mice if compared to controls. No difference was observed for IL-17, IL-23R, IL-36R or F480. Knowledge of the spatial–temporal pattern distribution of the pathological lesions of a well-characterized disease model lays the foundation for the study of the tissue expression of meaningful predictive biomarkers, thereby improving translational success rates of preclinical studies for a personalized management of IBD patients. Full article
(This article belongs to the Special Issue Molecular Research in Inflammatory Bowel Disease 2.0)
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21 pages, 3589 KiB  
Article
Lessons on the Sigma-1 Receptor in TNBS-Induced Rat Colitis: Modulation of the UCHL-1, IL-6 Pathway
by Nikoletta Almási, Szilvia Török, Szabolcs Dvorácskó, Csaba Tömböly, Ákos Csonka, Zoltán Baráth, Zsolt Murlasits, Zsuzsanna Valkusz, Anikó Pósa, Csaba Varga and Krisztina Kupai
Int. J. Mol. Sci. 2020, 21(11), 4046; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114046 - 05 Jun 2020
Cited by 14 | Viewed by 3472
Abstract
Inflammatory Bowel Disease (IBD) is an autoimmune ailment of the gastrointestinal (GI) tract, which is characterized by enhanced activation of proinflammatory cytokines. It is suggested that the sigma-1 receptor (σ1R) confers anti-inflammatory effects. As the exact pathogenesis of IBD is still unknown and [...] Read more.
Inflammatory Bowel Disease (IBD) is an autoimmune ailment of the gastrointestinal (GI) tract, which is characterized by enhanced activation of proinflammatory cytokines. It is suggested that the sigma-1 receptor (σ1R) confers anti-inflammatory effects. As the exact pathogenesis of IBD is still unknown and treatment options are limited, we aimed to investigate the effects of σ1R in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. To this end, male Wistar–Harlan rats were used to model colitic inflammation through the administration of TNBS. To investigate the effects of σ1R, Fluvoxamine (FLV, σ1R agonist) and BD1063 (σ1R antagonist) were applied via intracolonic administration to the animals once a day for three days. Our radioligand binding studies indicated the existence of σ1Rs as [3H](+)-pentazocine binding sites, and FLV treatment increased the reduced σ1R maximum binding capacity in TNBS-induced colitis. Furthermore, FLV significantly attenuated the colonic damage, the effect of which was abolished by the administration of BD1063. Additionally, FLV potentially increased the expression of ubiquitin C-terminal hydrolase ligase-1 (UCHL-1) and the levels of endothelial nitric oxide synthase (eNOS), and decreased the levels of interleukin-6 (IL-6) and inducible NOS (iNOS) expression. In summary, our study offers evidence for the anti-inflammatory potential of FLV and σ1R in experimental colitis, and our results present a promising approach to the development of new σ1R-targeted treatment options against IBD. Full article
(This article belongs to the Special Issue Molecular Research in Inflammatory Bowel Disease 2.0)
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13 pages, 2285 KiB  
Article
Dextran Sodium Sulfate-Induced Impairment of Protein Trafficking and Alterations in Membrane Composition in Intestinal Caco-2 Cell Line
by Mohamad Toutounji, Dalanda Wanes, Mohammad El-Harakeh, Marwan El-Sabban, Sandra Rizk and Hassan Y. Naim
Int. J. Mol. Sci. 2020, 21(8), 2726; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082726 - 15 Apr 2020
Cited by 17 | Viewed by 5664
Abstract
A key morphological feature of inflammatory bowel disease (IBD) is the loss of the barrier function of intestinal epithelial cells. The present study investigates endoplasmic reticulum (ER) stress in addition to alterations in protein and membrane trafficking in a dextran sulfate sodium (DSS)-induced [...] Read more.
A key morphological feature of inflammatory bowel disease (IBD) is the loss of the barrier function of intestinal epithelial cells. The present study investigates endoplasmic reticulum (ER) stress in addition to alterations in protein and membrane trafficking in a dextran sulfate sodium (DSS)-induced IBD-like phenotype of intestinal Caco-2 cells in culture. DSS treatment significantly reduced the transepithelial electric resistance (TEER) and increased the epithelial permeability of Caco-2 cells, without affecting their viability. This was associated with an alteration in the expression levels of inflammatory factors in addition to an increase in the expression of the ER stress protein markers, namely immunoglobulin-binding protein (BiP), C/EBP homologous protein (CHOP), activation transcription factor 4 (ATF4), and X-box binding protein (XBP1). The DSS-induced ER-stress resulted in impaired intracellular trafficking and polarized sorting of sucrase-isomaltase (SI) and dipeptidyl peptidase-4 (DPPIV), which are normally sorted to the apical membrane via association with lipid rafts. The observed impaired sorting was caused by reduced cholesterol levels and subsequent distortion of the lipid rafts. The data presented confirm perturbation of ER homeostasis in DSS-treated Caco-2 cells, accompanied by impairment of membrane and protein trafficking resulting in altered membrane integrity, cellular polarity, and hence disrupted barrier function. Full article
(This article belongs to the Special Issue Molecular Research in Inflammatory Bowel Disease 2.0)
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