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Inflammatory Bowel Disease: Molecular Advances in Pathogenesis and Therapies, 2nd Edition

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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: 25 December 2026 | Viewed by 1920

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Prof. Dr. Rafał Filip

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Guest Editor

1. Institute of Medicine, Medical College of Rzeszow University, 35-959 Rzeszow, Poland
2. Department of Gastroenterology with IBD Unit, Clinical Hospital No. 2, 35-301 Rzeszów, Poland
Interests: crohns disease; uIcerative colitis; GI endoscopy; GI immunology; gastrointestinal diseases
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Dr. Aneta Sokal-Dembowska

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Faculty of Health Sciences and Psychology, Collegium Medicum, University of Rzeszow, 35-959 Rzeszow, Poland
Interests: nutrition; gastrointestinal diseases; autoimmune diseases; public health
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Dr. Sara Jarmakiewicz-Czaja

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Guest Editor

Institute of Medicine, Medical College of Rzeszow University, 35-959 Rzeszow, Poland
Interests: gastrointestinal disease; gut microbiome; inflammatory bowel disease; nutrients; nutrition
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Special Issue Information

Dear Colleagues,

Inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, are chronic conditions characterized by alternating periods of activity and remission. Despite significant progress in understanding the etiology of IBD, it remains not fully elucidated. Nevertheless, numerous studies indicate that genetic, environmental, and immunological factors play key roles in the occurrence of these conditions. A deeper understanding of the molecular and immunological mechanisms involved in their pathogenesis may contribute to improved therapeutic strategies.

The purpose of this Special Issue is to deepen knowledge and gather information on the molecular and pathophysiological mechanisms of inflammatory bowel disease, as well as to present the current state of the field and its future prospects.

To ensure diversity in approaches and perspectives, we welcome various types of submissions, including original research articles, systematic reviews, and communication.

Prof. Dr. Rafał Filip
Dr. Aneta Sokal-Dembowska
Dr. Sara Jarmakiewicz-Czaja
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 250 words) can be sent to the Editorial Office for assessment.

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.

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Keywords

Crohn’s disease
inflammatory bowel disease
immunologic and molecular mechanisms
therapies in IBD
ulcerative colitis

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Inflammatory Bowel Disease: Molecular Advances in Pathogenesis and Therapies in International Journal of Molecular Sciences (18 articles)

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Research

15 pages, 4182 KB

Open AccessArticle

miR-369-3p Modulates LRRK2-Mediated Inflammation and Autophagy in RAW264.7 Macrophages

by Viviana Scalavino, Emanuele Piccinno, Ilaria Grassi, Raffaele Armentano, Gianluigi Giannelli and Grazia Serino

Int. J. Mol. Sci. 2026, 27(7), 3220; https://doi.org/10.3390/ijms27073220 - 2 Apr 2026

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Abstract

Leucine-rich-repeat kinase 2 (LRRK2) is a multidomain protein highly expressed in immune cells and implicated in the regulation of immune functions including immune signaling, cytokine release and autophagy. LRRK2 is one of the therapeutic targets in Parkinson’s Disease (PD). Aberrant activation of LRRK2 can also contribute to intestinal inflammation, mainly in inflammatory bowel disease (IBD). Hence the modulation of LRRK2 may influence gut inflammation providing an improvement in disease outcomes. Over the years, microRNAs (miRNAs) have acquired much attention thanks to their potential as therapeutic targets in several pathological conditions, including inflammatory disorders. In this study, we aimed to examine the ability of miR-369-3p in the modulation of autophagy targeting LRRK2 expression. Bioinformatics analysis revealed that Lrrk2 is a target gene of miR-369-3p, and LRRK2 expression was increased in ulcerative colitis patients compared with that in a healthy control. In in vitro analysis, we validated that mimic transfection with miR-369-3p in Raw264.7 significantly reduced the expression of LRRK2 both in basal and inflammatory conditions. Moreover, the inhibition of LRRK2 limited the nuclear translocation of Nuclear factor kappa B (NF-κB) induced by lipopolysaccharide (LPS) stimulation. In turn, we found that, in inflammatory conditions, the intracellular increase in miR-369-3p precluded the inhibition of autophagy by LRRK2 by restoring autophagy marker light chain 3 (LC3)II/I ratio, BECLIN-1 and decreasing p62 expression. Furthermore, we detected that the upregulation of miR-369-3p decreased the release of pro-inflammatory mediators Tumor necrosis factor (TNF), C-C motif ligand 2/Monocyte chemoattractant protein-1 (CCL2/MCP-1), C-C motif ligand 3/Macrophage inflammatory protein-1 alpha (CCL3/MIP-1α) and C-C motif ligand 5/Regulated on activation, normal T-cell expressed and secreted (CCL5/RANTES) and increased the anti-inflammatory cytokine interleukin 10 (IL-10) in response to LPS. This study supports the anti-inflammatory potential of miR-369-3p in immune cells and suggests the potential of miR-369-3p as a therapeutic agent in the treatment of acute intestinal inflammatory conditions such as ulcerative colitis. Full article

(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Advances in Pathogenesis and Therapies, 2nd Edition)

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18 pages, 2948 KB

Open AccessArticle

Anti-Inflammatory Potential of Novel Tethered Agonists of the Adhesion G Protein-Coupled Receptor F5

by Artur Wnorowski, Diana Pietrzak-Mitura, Akanksha Mudgal, Lorenzo Scrofani, Magdalena Strachowska, Piotr Draczkowski, Krzysztof Jóźwiak, Jakub Fichna and Damian Jacenik

Int. J. Mol. Sci. 2026, 27(6), 2648; https://doi.org/10.3390/ijms27062648 - 13 Mar 2026

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Abstract

The adhesion G protein-coupled receptor F5 (ADGRF5) has been implicated in modulating immune responses in cancer; however, its role in inflammatory bowel diseases (IBDs), particularly colitis, remains largely unexplored. In this study, we aimed to design and characterize novel peptide agonists derived from the ADGRF5 Stachel sequence, as well as to evaluate their therapeutic potential in preclinical colitis models. In silico analysis and single amino acid substitutions within the ADGRF5 tethered agonist sequence, combined with functional assays in ADGRF5-overexpressing cells, including calcium mobilization and inositol phosphate production, were employed to assess the activity of novel ADGRF5 agonists. Western blot technique and murine model of colitis were used to evaluate downstream signaling pathways and immunomodulatory effects of ADGRF5 ligands. We identified a series of peptides exhibiting significantly enhanced ADGRF5 agonist activity, achieving up to a 6-fold increase in potency over the wild-type version. We identified critical substitutions within the Stachel sequence, namely S11N and D13S, as essential for improving agonistic activity. Finally, using these novel ADGRF5 agonists, we demonstrated their potent anti-inflammatory effects in vivo, showing that ADGRF5 activation ameliorates experimental colitis, as evidenced by reduced macroscopic damage scores and improved colon architecture. These findings establish ADGRF5 as a potential therapeutic target for colitis and highlight the promise of Stachel-derived peptide agonists for the development of novel anti-inflammatory therapies. Full article

(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Advances in Pathogenesis and Therapies, 2nd Edition)

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17 pages, 7919 KB

Open AccessArticle

Etrasimod Treatment Modulates Circulating and Lymph Node-Derived Lymphocytes in Crohn’s Disease

by Dimitrios Nikolakis, Maarten J. Pruijt, Jan Verhoeff, Floris A. E. de Voogd, Christoph Teichert, Rathi D. Ryan, Diogo Branquinho, Catherine Crosby, Marleen G. H. van de Sande, Joep Grootjans and Geert R. D’Haens

Int. J. Mol. Sci. 2026, 27(5), 2447; https://doi.org/10.3390/ijms27052447 - 6 Mar 2026

Viewed by 430

Abstract

Etrasimod is an oral selective sphingosine-1 phosphate receptor modulator, and its anti-inflammatory mechanism of action in inflammatory bowel diseases is not completely understood. It targets pro-inflammatory immune cells expressing sphingosine-1-phosphate receptors during their migration from the lymphatic system to the circulation and intestinal mucosa. Reductions in certain lymphocyte subsets in the peripheral blood have been reported, but its effects in lymph nodes remain unknown. This study investigated changes in leukocyte subpopulations in peripheral lymph nodes and blood in Crohn’s disease patients treated with etrasimod. Moderate-to-severe Crohn’s disease patients participated in this randomized, double-blind study, within the phase 2 CULTIVATE clinical trial. At baseline and after 14 weeks of etrasimod treatment, peripheral blood and inguinal lymph node biopsies were obtained. Isolated peripheral blood mononuclear cells and lymph node leukocyte populations were analyzed at single cell level using mass cytometry at both timepoints. The immunophenotyping revealed 15 innate and adaptive major immune cell populations, as well as 14 subpopulations of CD4+ and CD8+ T-cells. In peripheral lymph nodes, etrasimod resulted in significant accumulation of naïve, central memory, and effector memory CD4+ T-cells (+10.7%, +4.2%, and +2.3%, respectively; all p = 0.03), as well as naïve CD8+ T-cells (+4.2%; p = 0.03). Conversely, these subsets were reduced in peripheral blood (−6.2%, −6.0%, −2.0%, and −2.2%, respectively; all p = 0.03). Naïve and memory B-cells decreased in the circulation (−1.7%, p = 0.057; −0.6%, p = 0.03, respectively) but were unchanged in the lymph nodes. Innate immune cell populations remained mostly unaffected in both compartments. Our data indicate that etrasimod’s pharmacodynamic effect is related primarily with the attenuation of the T-cell mediated inflammation with minor changes in B-cells. However, additional follow-up studies are needed for the validation of these observations in the context of Crohn’s disease. Full article

(This article belongs to the Special Issue Inflammatory Bowel Disease: Molecular Advances in Pathogenesis and Therapies, 2nd Edition)

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