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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 February 2025 | Viewed by 7184

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

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Published Papers (6 papers)

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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
Viewed by 1420
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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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
Viewed by 1399
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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21 pages, 1264 KiB  
Review
The Role of Host Genetics and Intestinal Microbiota and Metabolome as a New Insight into IBD Pathogenesis
by Oliwia Zakerska-Banaszak, Joanna Zuraszek-Szymanska, Piotr Eder, Karolina Ladziak, Ryszard Slomski and Marzena Skrzypczak-Zielinska
Int. J. Mol. Sci. 2024, 25(17), 9589; https://doi.org/10.3390/ijms25179589 - 4 Sep 2024
Viewed by 1337
Abstract
Inflammatory bowel disease (IBD) is an incurable, chronic disorder of the gastrointestinal tract whose incidence increases every year. Scientific research constantly delivers new information about the disease and its multivariate, complex etiology. Nevertheless, full discovery and understanding of the complete mechanism of IBD [...] Read more.
Inflammatory bowel disease (IBD) is an incurable, chronic disorder of the gastrointestinal tract whose incidence increases every year. Scientific research constantly delivers new information about the disease and its multivariate, complex etiology. Nevertheless, full discovery and understanding of the complete mechanism of IBD pathogenesis still pose a significant challenge to today’s science. Recent studies have unanimously confirmed the association of gut microbial dysbiosis with IBD and its contribution to the regulation of the inflammatory process. It transpires that the altered composition of pathogenic and commensal bacteria is not only characteristic of disturbed intestinal homeostasis in IBD, but also of viruses, parasites, and fungi, which are active in the intestine. The crucial function of the microbial metabolome in the human body is altered, which causes a wide range of effects on the host, thus providing a basis for the disease. On the other hand, human genomic and functional research has revealed more loci that play an essential role in gut homeostasis regulation, the immune response, and intestinal epithelial function. This review aims to organize and summarize the currently available knowledge concerning the role and interaction of crucial factors associated with IBD pathogenesis, notably, host genetic composition, intestinal microbiota and metabolome, and immune regulation. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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15 pages, 1937 KiB  
Article
Chemokinergic and Dopaminergic Signalling Collaborates through the Heteromer Formed by CCR9 and Dopamine Receptor D5 Increasing the Migratory Speed of Effector CD4+ T-Cells to Infiltrate the Colonic Mucosa
by Javier Campos, Francisco Osorio-Barrios, Felipe Villanelo, Sebastian E. Gutierrez-Maldonado, Pablo Vargas, Tomás Pérez-Acle and Rodrigo Pacheco
Int. J. Mol. Sci. 2024, 25(18), 10022; https://doi.org/10.3390/ijms251810022 - 18 Sep 2024
Viewed by 817
Abstract
Inflammatory bowel diseases (IBDs) involve chronic inflammation of the gastrointestinal tract, where effector CD4+ T-cells play a central role. Thereby, the recruitment of T-cells into the colonic mucosa represents a key process in IBD. We recently found that CCR9 and DRD5 might [...] Read more.
Inflammatory bowel diseases (IBDs) involve chronic inflammation of the gastrointestinal tract, where effector CD4+ T-cells play a central role. Thereby, the recruitment of T-cells into the colonic mucosa represents a key process in IBD. We recently found that CCR9 and DRD5 might form a heteromeric complex on the T-cell surface. The increase in CCL25 production and the reduction in dopamine levels associated with colonic inflammation represent a dual signal stimulating the CCR9:DRD5 heteromer, which promotes the recruitment of CD4+ T-cells into the colonic lamina propria. Here, we aimed to analyse the molecular requirements involved in the heteromer assembly as well as to determine the underlying cellular mechanisms involved in the colonic tropism given by the stimulation of the CCR9:DRD5 complex. The results show that dual stimulation of the CCR9:DRD5 heteromer potentiates the phosphorylation of the myosin light chain 2 (MLC2) and the migration speed in confined microchannels. Accordingly, disrupting the CCR9:DRD5 assembly induced a sharp reduction in the pMLC2 in vitro, decreased the migratory speed in confined microchannels, and dampened the recruitment of CD4+ T-cells into the inflamed colonic mucosa. Furthermore, in silico analysis confirmed that the interface of interaction of CCR9:DRD5 is formed by the transmembrane segments 5 and 6 from each protomer. Our findings demonstrated that the CCR9:DRD5 heteromeric complex plays a fundamental role in the migration of CD4+ T-cells into the colonic mucosa upon inflammation. Thereby, the present study encourages the design of strategies for disassembling the formation of the CCR9:DRD5 as a therapeutic opportunity to treat IBD. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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17 pages, 3070 KiB  
Article
Involvement of Intestinal Epithelium Aryl Hydrocarbon Receptor Expression and 3, 3′-Diindolylmethane in Colonic Tertiary Lymphoid Tissue Formation
by Erika L. Garcia-Villatoro, Zachary S. Bomstein, Kimberly F. Allred, Evelyn S. Callaway, Stephen Safe, Robert S. Chapkin, Arul Jayaraman and Clinton D. Allred
Int. J. Mol. Sci. 2024, 25(18), 10153; https://doi.org/10.3390/ijms251810153 - 21 Sep 2024
Viewed by 878
Abstract
Tertiary lymphoid tissues (TLTs) are adaptive immune structures that develop during chronic inflammation and may worsen or lessen disease outcomes in a context-specific manner. Immune cell activity governing TLT formation in the intestines is dependent on immune cell aryl hydrocarbon receptor (AhR) activation. [...] Read more.
Tertiary lymphoid tissues (TLTs) are adaptive immune structures that develop during chronic inflammation and may worsen or lessen disease outcomes in a context-specific manner. Immune cell activity governing TLT formation in the intestines is dependent on immune cell aryl hydrocarbon receptor (AhR) activation. Homeostatic immune cell activity in the intestines is further dependent on ligand activation of AhR in intestinal epithelial cells (IECs), yet whether AhR activation and signaling in IECs influences the formation of TLTs in the presence of dietary AhR ligands is not known. To this end, we used IEC-specific AhR deletion coupled with a mouse model of dextran sodium sulfate (DSS)-induced colitis to understand how dietary AhR ligand 3, 3′-diindolylmethane (DIM) influenced TLT formation. DIM consumption increased the size of TLTs and decreased T-cell aggregation to TLT sites in an IEC-specific manner. In DSS-exposed female mice, DIM consumption increased the expression of genes implicated in TLT formation (Interleukin-22, Il-22; CXC motif chemokine ligand 13, CXCL13) in an IEC AhR-specific manner. Conversely, in female mice without DSS exposure, DIM significantly reduced the expression of Il-22 or CXCL13 in iAhRKO mice, but this effect was not observed in WT animals. Our findings suggest that DIM affects the immunological landscape of TLT formation during DSS-induced colitis in a manner contingent on AhR expression in IECs and biological sex. Further investigations into specific immune cell activity, IEC-specific AhR signaling pathways, and dietary AhR ligand-mediated effects on TLT formation are warranted. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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14 pages, 3728 KiB  
Article
Microsomal Prostaglandin E Synthase-1 Controls Colonic Prostaglandin E2 Production and Exerts a Protective Effect on Colitis Induced by Trinitrobenzene Sulfonic Acid in Mice
by Fumiaki Kojima, Yuka Hioki, Hiroki Sekiya, Hitoshi Kashiwagi, Yoshiko Iizuka, Kei Eto, Shotaro Maehana, Fumitaka Kawakami, Makoto Kubo, Hitoshi Ishibashi and Takafumi Ichikawa
Int. J. Mol. Sci. 2024, 25(22), 12326; https://doi.org/10.3390/ijms252212326 - 17 Nov 2024
Viewed by 272
Abstract
Microsomal prostaglandin E synthase-1 (mPGES-1) is an isozyme of the prostaglandin (PG) E synthase that acts downstream of cyclooxygenase and catalyzes the conversion of PGH2 to PGE2. The impact of genetic deletion of mPGES-1 on the development of 2,4,6-trinitrobenzene sulfonic [...] Read more.
Microsomal prostaglandin E synthase-1 (mPGES-1) is an isozyme of the prostaglandin (PG) E synthase that acts downstream of cyclooxygenase and catalyzes the conversion of PGH2 to PGE2. The impact of genetic deletion of mPGES-1 on the development of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, a well-established model of inflammatory bowel disease (IBD), was investigated in this study. After administration of TNBS, mice deficient in mPGES-1 (mPGES-1−/− mice) showed more severe colitis than did wild-type (WT) mice. Histological examination revealed that mPGES-1−/− mice had markedly exacerbated symptoms of colitis. mPGES-1 expression was detectable in the colons of WT mice at both the mRNA and protein levels. Lack of mPGES-1 resulted in marked reduction of colonic PGE2 production. Our study also showed a significant increase in colonic expression of interleukin-17A (IL-17A), as well as interferon γ (IFNγ) and tumor necrosis factor α, during colitis in mPGES-1−/− mice compared with that in WT mice. Furthermore, loss of mPGES-1 increased the populations of IL-17A-producing T-helper (Th) 17 and IFNγ-producing Th1 cells in mesenteric lymph nodes. These results suggest that mPGES-1 is the main enzyme responsible for colonic PGE2 production and deficiency of mPGES-1 facilitates the development of colitis and T-cell-mediated immunity. mPGES-1 might, therefore, impact T-cell-related immune response associated with IBD. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Insights)
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