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Inflammatory Bowel Disease: Molecular Insights
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Inflammatory Bowel Disease: Molecular Insights

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: 20 September 2024 | Viewed by 1794

Special Issue Editor

Dr. Belal Chami

E-Mail Website
Guest Editor
1. Discipline of Pathology, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, Sydney, NSW 2006, Australia
2. Charles Perkins Centre, The University of Sydney, Camperdown, Sydney, NSW 2006, Australia
Interests: inflammatory bowel disease; neutrophils; myeloperoxidase; inflammation; colitis; redox biology; antioxidants; reactive oxygen species; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory Bowel Disease is an elusive gastrointestinal inflammatory disease of chronicity, which in many cases diminishes the quality of life of sufferers. While the armamentarium of therapeutic pharmacologies is ever expanding, our understanding of the molecular underpinnings to this insidious disease lags behind. If we are to progress to curative therapies, we must first define the molecular signatures of IBD at the genetic, biochemical and immunobiological level. This will likely include the complex interaction of a multitude of cells, messenger substances and proteins within the gut environment, immune-related structures and systemic circulation.

Recent advancements in genomic technologies, high-throughput imaging mass spectrometry and multiomic analysis have progressed our understanding of the interplay of endogenous and exogenous factors through newly discovered molecular actors, improved understanding of microbiome dysbiosis and spatial immunocompartmentalisation of the IBD-affected gut. This forms the aims of the Special Issue ‘Inflammatory Bowel Disease: Molecular Insights’.

As a longstanding IBD researcher, it is my pleasure to invite you all to contribute to the Special Issue ‘Inflammatory Bowel Disease: Molecular Insights’ for the journal International Journal for Molecular Sciences (impact factor 5.6).

We are welcoming original research manuscripts that help to unravel exciting and novel findings which have the potential to shed light on the pathogenesis of IBD.

The scope of this issue includes research relating to human multiomic analysis, genomic sequencing, studies with components of basic science research or mechanistic data and animal studies with relevance to Crohn’s disease and/or ulcerative colitis.

I look forward to receiving your original research.

Dr. Belal Chami
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

  • genomic sequencing
  • microbiome
  • dysbiosis
  • commensal flora
  • omics
  • immunobiology
  • colitis
  • Crohn’s disease
  • ulcerative colitis
  • multiomics

Published Papers (2 papers)

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14 pages, 2939 KiB  
Article
Myeloperoxidase Gene Deletion Causes Drastic Microbiome Shifts in Mice and Does Not Mitigate Dextran Sodium Sulphate-Induced Colitis
by Patrick T. San Gabriel, Thomas R. O’Neil, Alice Au, Jian K. Tan, Gabriela V. Pinget, Yuyang Liu, Genevieve Fong, Jacqueline Ku, Elias Glaros, Laurence Macia, Paul K. Witting, Shane R. Thomas and Belal Chami
Int. J. Mol. Sci. 2024, 25(8), 4258; https://doi.org/10.3390/ijms25084258 - 11 Apr 2024
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Abstract
Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the role of MPO using knockout (KO) models. Therefore, we investigated MPO deficient mice [...] Read more.
Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the role of MPO using knockout (KO) models. Therefore, we investigated MPO deficient mice in a murine model of colitis. Wild type (Wt) and MPO-deficient mice were treated with dextran sodium sulphate (DSS) in a chronic model of experimental colitis with three acute cycles of DSS-induced colitis over 63 days, emulating IBD relapse and remission cycles. Mice were immunologically profiled at the gut muscoa and the faecal microbiome was assessed via 16S rRNA amplicon sequencing. Contrary to previous pharmacological antagonist studies targeting MPO, MPO-deficient mice showed no protection from experimental colitis during cyclical DSS-challenge. We are the first to report drastic faecal microbiota shifts in MPO-deficient mice, showing a significantly different microbiome profile on Day 1 of treatment, with a similar shift and distinction on Day 29 (half-way point), via qualitative and quantitative descriptions of phylogenetic distances. Herein, we provide the first evidence of substantial microbiome shifts in MPO-deficiency, which may influence disease progression. Our findings have significant implications for the utility of MPO-KO mice in investigating disease models. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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12 pages, 1371 KiB  
Article
A Prospective Observational Study Analyzing the Diagnostic Value of Hepcidin-25 for Anemia in Patients with Inflammatory Bowel Diseases
by Stanko Petrović, Dino Tarabar, Danica Ćujić, Dusica Stamenkovic, Marijana Petrović, Nemanja Rančić, Vesna Subota, Nenad Perišić and Mihailo Bezmarević
Int. J. Mol. Sci. 2024, 25(7), 3564; https://doi.org/10.3390/ijms25073564 - 22 Mar 2024
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Abstract
Iron deficiency (IDA) and chronic disease (ACD) anemia are complications of inflammatory bowel diseases (IBDs). Therapeutic modalities in remission and active IBD depend on the type of anemia. This study evaluated the link between hepcidin-25, proinflammatory cytokines, and platelet activation markers as biomarkers [...] Read more.
Iron deficiency (IDA) and chronic disease (ACD) anemia are complications of inflammatory bowel diseases (IBDs). Therapeutic modalities in remission and active IBD depend on the type of anemia. This study evaluated the link between hepcidin-25, proinflammatory cytokines, and platelet activation markers as biomarkers of anemia and inflammation in active IBD and remission. This prospective observational study included 62 patients with IBD (49 with ulcerative colitis and 13 with Crohn’s) and anemia. Patients were divided into Group I (no or minimal endoscopic signs of disease activity and IDA), Group II (moderate and major endoscopic signs of disease activity and mild ACD), and Control group (10 patients with IBD in remission, without anemia). We assessed the difference among groups in the levels of CRP, hemoglobin (Hgb), serum iron, ferritin, hepcidin-25, interleukins, TNF–α, IFN-γ, soluble CD40 ligand, and sP-selectin. Hepcidin-25 levels were significantly higher in Group II versus Group I (11.93 vs. 4.48 ng/mL, p < 0.001). Ferritin and CRP values showed similar patterns in IBD patients: significantly higher levels were observed in Group II (47.5 ng/mL and 13.68 mg/L) than in Group I (11.0 ng/mL and 3.39 mg/L) (p < 0.001). In Group II, hepcidin-25 was positively correlated with ferritin (ρ = 0.725, p < 0.001) and CRP (ρ = 0.502, p = 0.003). Ferritin was an independent variable influencing hepcidin-25 concentration in IBD patients, regardless of disease activity and severity of anemia. IBD hepcidin-25 best correlates with ferritin, and both parameters reflected inflammation extent and IBD activity. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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