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Cells
Special Issues
Therapeutic Strategies for Treatment of Inflammatory Bowel Disease
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Therapeutic Strategies for Treatment of Inflammatory Bowel Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (20 May 2023) | Viewed by 7963

Special Issue Editors

Prof. Dr. Jørgen Olsen

E-Mail Website
Guest Editor
Department of Cellular and Molecular Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Interests: inflammatory bowel disease; rectal insulin treatment; insulin signaling in the colonocyte; intestinal development and morphogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Gerhard Rogler

E-Mail Website
Guest Editor
Department of Gastroenterology and Hepatology, University Hospital Zurich, University of Zurich, 8091 Zurich, Switzerland
Interests: inflammatody bowel disease; clinical trials; IBD therapy
Dr. Jacob Bjerrum

E-Mail Website
Guest Editor
Department of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark
Interests: inflammatory bowel disease; metabonomics; transcriptomics

Special Issue Information

Dear Colleagues,

In recent years, the inflammatory bowel disease community has witnessed the marketing of novel therapies involving orally administrated drugs that target key inflammatory signaling pathways. This is an important development for patients. However, these carefully designed drugs do not cure inflammatory bowel disease; moreover, the active pharmaceutical ingredients have serious side effects, and a sub-group of patients are not responsive to them. Thus, given the personal and societal impact of this disease, this unmet need warrants the continued development of novel therapeutic strategies for the treatment of inflammatory bowel disease.

Prof. Dr. Jørgen Olsen
Prof. Dr. Gerhard Rogler
Dr. Jacob Bjerrum
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • microbiota
  • drug repurposing
  • JAK kinase inhibitors
  • biologics
  • sphingosine kinase inhibitors
  • antioxidants

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Published Papers (3 papers)

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Research

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23 pages, 21521 KiB  
Article
Butyrate Protects Myenteric Neurons Loss in Mice Following Experimental Ulcerative Colitis
by Marcos A. F. Caetano, Henrique I. R. Magalhães, Jheniffer R. L. Duarte, Laura B. Conceição and Patricia Castelucci
Cells 2023, 12(13), 1672; https://doi.org/10.3390/cells12131672 - 21 Jun 2023
Cited by 4 | Viewed by 1704
Abstract
The enteric nervous system is affected by inflammatory bowel diseases (IBD). Gut microbiota ferments dietary fibers and produces short-chain fatty acids, such as Butyrate, which bind to G protein–coupled receptors, such as GPR41, and contribute to maintaining intestinal health. This work aimed to [...] Read more.
The enteric nervous system is affected by inflammatory bowel diseases (IBD). Gut microbiota ferments dietary fibers and produces short-chain fatty acids, such as Butyrate, which bind to G protein–coupled receptors, such as GPR41, and contribute to maintaining intestinal health. This work aimed to study the GPR41 in myenteric neurons and analyze the effect of Butyrate in mice submitted to experimental ulcerative colitis. The 2, 4, 6 trinitrobenzene sulfonic acid (TNBS) was injected intrarectally in C57BL/6 mice (Colitis). Sham group received ethanol (vehicle). One group was treated with 100 mg/kg of Sodium Butyrate (Butyrate), and the other groups received saline. Animals were euthanized 7 days after colitis induction. Analyzes demonstrated colocalization of GPR41 with neurons immunoreactive (-ir) to nNOS and ChAT-ir and absence of colocalization of the GPR41 with GFAP-ir glia. Quantitative results demonstrated losses of nNOS-ir, ChAT-ir, and GPR41-ir neurons in the Colitis group and Butyrate treatment attenuated neuronal loss. The number of GFAP-ir glia increased in the Colitis group, whereas Butyrate reduced the number of these cells. In addition, morphological alterations observed in the Colitis group were attenuated in the Butyrate group. The presence of GPR41 in myenteric neurons was identified, and the treatment with Butyrate attenuated the damage caused by experimental ulcerative colitis. Full article
(This article belongs to the Special Issue Therapeutic Strategies for Treatment of Inflammatory Bowel Disease)
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Review

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29 pages, 1757 KiB  
Review
Circular and Circulating DNA in Inflammatory Bowel Disease: From Pathogenesis to Potential Molecular Therapies
by Federica Di Vincenzo, Ylenia Yadid, Valentina Petito, Valeria Emoli, Letizia Masi, Daniela Gerovska, Marcos Jesus Araúzo-Bravo, Antonio Gasbarrini, Birgitte Regenberg and Franco Scaldaferri
Cells 2023, 12(15), 1953; https://doi.org/10.3390/cells12151953 - 27 Jul 2023
Cited by 4 | Viewed by 2938
Abstract
Inflammatory bowel diseases (IBD), including Crohn’s Disease (CD) and Ulcerative Colitis (UC) are chronic multifactorial disorders which affect the gastrointestinal tract with variable extent. Despite extensive research, their etiology and exact pathogenesis are still unknown. Cell-free DNAs (cfDNAs) are defined as any DNA [...] Read more.
Inflammatory bowel diseases (IBD), including Crohn’s Disease (CD) and Ulcerative Colitis (UC) are chronic multifactorial disorders which affect the gastrointestinal tract with variable extent. Despite extensive research, their etiology and exact pathogenesis are still unknown. Cell-free DNAs (cfDNAs) are defined as any DNA fragments which are free from the origin cell and able to circulate into the bloodstream with or without microvescicles. CfDNAs are now being increasingly studied in different human diseases, like cancer or inflammatory diseases. However, to date it is unclear how IBD etiology is linked to cfDNAs in plasma. Extrachromosomal circular DNA (eccDNA) are non-plasmidic, nuclear, circular and closed DNA molecules found in all eukaryotes tested. CfDNAs appear to play an important role in autoimmune diseases, inflammatory processes, and cancer; recently, interest has also grown in IBD, and their role in the pathogenesis of IBD has been suggested. We now suggest that eccDNAs also play a role in IBD. In this review, we have comprehensively collected available knowledge in literature regarding cfDNA, eccDNA, and structures involving them such as neutrophil extracellular traps and exosomes, and their role in IBD. Finally, we focused on old and novel potential molecular therapies and drug delivery systems, such as nanoparticles, for IBD treatment. Full article
(This article belongs to the Special Issue Therapeutic Strategies for Treatment of Inflammatory Bowel Disease)
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12 pages, 1467 KiB  
Review
Novel Small Molecules in IBD: Current State and Future Perspectives
by André Jefremow and Markus F. Neurath
Cells 2023, 12(13), 1730; https://doi.org/10.3390/cells12131730 - 27 Jun 2023
Cited by 7 | Viewed by 2923
Abstract
Biologicals have dominated the therapeutic scenery in inflammatory bowel diseases (IBDs), namely ulcerative colitis (UC) and Crohn’s disease (CD), for the past 20 years. The development of tofacitinib was the starting point for an era of small molecules after the era of biologicals. [...] Read more.
Biologicals have dominated the therapeutic scenery in inflammatory bowel diseases (IBDs), namely ulcerative colitis (UC) and Crohn’s disease (CD), for the past 20 years. The development of tofacitinib was the starting point for an era of small molecules after the era of biologicals. These new agents may challenge the use of biological agents in the future. They share properties that appeal to both patients and physicians. Low production costs, a lack of immunogenicity, and ease of use are only some of their benefits. On the other hand, patients and their physicians must manage the potential side effects of small molecules such as JAK inhibitors or S1P1R modulators. Here, we present agents that have already entered the clinical routine and those that are still being investigated in clinical trials. Full article
(This article belongs to the Special Issue Therapeutic Strategies for Treatment of Inflammatory Bowel Disease)
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