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Molecular Diagnosis and Treatment of Inflammatory Bowel Disease
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Molecular Diagnosis and Treatment of Inflammatory Bowel Disease

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 June 2024 | Viewed by 4203

Special Issue Editor

Dr. Lidia V. Boldyreva

E-Mail Website
Guest Editor
Research Institute for Neurosciences & Medicine, 630117 Novosibirsk, Russia
Interests: molecular genetics; inflammatory bowel disease; genetics of neuronal processes; gut-brain axis; epigenetics; regulation of gene expression; functional genomics; animal models

Special Issue Information

Dear Colleagues,

IBD encompasses gastrointestinal tract disorders with a distinct set of clinical symptoms resulting from chronic inflammation and metabolic deregulation and characterized by serious impairment of the intestinal microbiota composition. Molecular studies demonstrate high heterogeneity of the IBD mechanisms. Despite the significant progress in understanding the etiology and development of treatment strategies, IBD remains incurable for thousands of patients. Thus, personalized approaches development for the diagnosis and treatment of IBD is highly relevant. On the other hand, generalization and the refining of IBD molecular markers are of great importance also. The identification of key IBD molecular triggers is the focus of the current research. The three main areas of interest for molecular treatment options for IBD are: mucosal and systemic immunity, the gut epithelial barrier, and the gut microbiome. Finding targeted means to normalize each of these functions provides ulterior perspectives in IBD therapy. This Special Issue invites research papers to highlight IBD molecular markers and pathways involved and outline perspectives for personalized IBD diagnosis and treatment. Systemizing reviews on these topics are also warmly welcome.

Dr. Lidia V. Boldyreva
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

  • inflammatory bowel disease
  • Crohn’s disease
  • ulcerative colitis
  • leaky gut
  • intestinal epithelial barrier
  • gastrointestinal microbiota
  • infection and inflammation
  • inflammatory pathways
  • molecular diagnosis
  • genetic variants related to IBD
  • IBD treatment
  • therapeutic resistance
  • targeted therapy
  • biological therapy
  • personalized IBD therapies
  • P4 medicine

Published Papers (4 papers)

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Research

13 pages, 1921 KiB  
Article
Protective Effects of Inulin on Stress-Recurrent Inflammatory Bowel Disease
by Yao Du, Kanta Kusama, Koki Hama, Xinyue Chen, Yu Tahara, Susumu Kajiwara, Shigenobu Shibata and Kanami Orihara
Int. J. Mol. Sci. 2024, 25(5), 2494; https://doi.org/10.3390/ijms25052494 - 21 Feb 2024
Viewed by 768
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the digestive tract and is closely associated with the homeostasis of the gut microbiota. Inulin, as a natural prebiotic, displays anti-inflammatory activity and maintains equilibrium of the intestinal microbiota. In this study, our [...] Read more.
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the digestive tract and is closely associated with the homeostasis of the gut microbiota. Inulin, as a natural prebiotic, displays anti-inflammatory activity and maintains equilibrium of the intestinal microbiota. In this study, our research aimed to explore the potential of inulin in enhancing intestinal immunity and reducing inflammation in stress-recurrent IBD. In this study, a co-culture intestinal epithelium model and a stress-recurrent IBD mouse model was used to examine the protective effects of inulin. It was observed that inulin digesta significantly reduced pro-inflammatory cytokine expression (CXCL8/IL8 and TNFA) and increased MUC2 expression in intestinal epithelial cells. In vivo, our findings showed that Inulin intake significantly prevented IBD symptoms. This was substantiated by a decrease in serum inflammatory markers (IL-6, CALP) and a downregulation of inflammatory cytokine (Il6) in colon samples. Additionally, inulin intake led to an increase in short-chain fatty acids (SCFAs) in cecal contents and a reduction in the expression of endoplasmic reticulum (ER) stress markers (CHOP, BiP). Our results highlight that inulin can improve stress-recurrent IBD symptoms by modulating microbiota composition, reducing inflammation, and alleviating ER stress. These findings suggested the therapeutic potential of inulin as a dietary intervention for ameliorating stress-recurrent IBD. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Inflammatory Bowel Disease)
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17 pages, 3796 KiB  
Article
Changes in HLA-B27 Transgenic Rat Fecal Microbiota Following Tofacitinib Treatment and Ileocecal Resection Surgery: Implications for Crohn’s Disease Management
by Aurélie Blondeaux, Caroline Valibouze, Silvia Speca, Christel Rousseaux, Caroline Dubuquoy, Hélène Blanquart, Philippe Zerbib, Pierre Desreumaux, Benoît Foligné and Marie Titécat
Int. J. Mol. Sci. 2024, 25(4), 2164; https://doi.org/10.3390/ijms25042164 - 10 Feb 2024
Viewed by 690
Abstract
The therapeutic management of Crohn’s disease (CD), a chronic relapsing–remitting inflammatory bowel disease (IBD), is highly challenging. Surgical resection is sometimes a necessary procedure even though it is often associated with postoperative recurrences (PORs). Tofacitinib, an orally active small molecule Janus kinase inhibitor, [...] Read more.
The therapeutic management of Crohn’s disease (CD), a chronic relapsing–remitting inflammatory bowel disease (IBD), is highly challenging. Surgical resection is sometimes a necessary procedure even though it is often associated with postoperative recurrences (PORs). Tofacitinib, an orally active small molecule Janus kinase inhibitor, is an anti-inflammatory drug meant to limit PORs in CD. Whereas bidirectional interactions between the gut microbiota and the relevant IBD drug are crucial, little is known about the impact of tofacitinib on the gut microbiota. The HLA-B27 transgenic rat is a good preclinical model used in IBD research, including for PORs after ileocecal resection (ICR). In the present study, we used shotgun metagenomics to first delineate the baseline composition and determinants of the fecal microbiome of HLA-B27 rats and then to evaluate the distinct impact of either tofacitinib treatment, ileocecal resection or the cumulative effect of both interventions on the gut microbiota in these HLA-B27 rats. The results confirmed that the microbiome of the HLA-B27 rats was fairly different from their wild-type littermates. We demonstrated here that oral treatment with tofacitinib does not affect the gut microbial composition of HLA-B27 rats. Of note, we showed that ICR induced an intense loss of bacterial diversity together with dramatic changes in taxa relative abundances. However, the oral treatment with tofacitinib neither modified the alpha-diversity nor exacerbated significant modifications in bacterial taxa induced by ICR. Collectively, these preclinical data are rather favorable for the use of tofacitinib in combination with ICR to address Crohn’s disease management when considering microbiota. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Inflammatory Bowel Disease)
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15 pages, 17167 KiB  
Article
Mucin Expression Profiles in Ulcerative Colitis: New Insights on the Histological Mucosal Healing
by Giuseppe Leoncini, Luigi Cari, Simona Ronchetti, Francesco Donato, Laura Caruso, Cristina Calafà and Vincenzo Villanacci
Int. J. Mol. Sci. 2024, 25(3), 1858; https://doi.org/10.3390/ijms25031858 - 03 Feb 2024
Cited by 1 | Viewed by 928
Abstract
A structural weakness of the mucus barrier (MB) is thought to be a cause of ulcerative colitis (UC). This study aims to investigate the mucin (MUC) composition of MB in normal mucosa and UC. Ileocolonic biopsies were taken at disease onset and after [...] Read more.
A structural weakness of the mucus barrier (MB) is thought to be a cause of ulcerative colitis (UC). This study aims to investigate the mucin (MUC) composition of MB in normal mucosa and UC. Ileocolonic biopsies were taken at disease onset and after treatment in 40 patients, including 20 with relapsing and 20 with remitting UC. Ileocolonic biopsies from 10 non-IBD patients were included as controls. Gut-specific MUC1, MUC2, MUC4, MUC5B, MUC12, MUC13, MUC15, and MUC17 were evaluated immunohistochemically. The promoters of mucin genes were also examined. Normal mucosa showed MUC2, MUC5B, and MUC13 in terminal ileum and colon, MUC17 in ileum, and MUC1, MUC4, MUC12, and MUC15 in colon. Membranous, cytoplasmic and vacuolar expressions were highlighted. Overall, the mucin expression was abnormal in UC. Derangements in MUC1, MUC4, and MUC5B were detected both at onset and after treatment. MUC2 and MUC13 were unaffected. Sequence analysis revealed glucocorticoid-responsive elements in the MUC1 promoter, retinoic-acid-responsive elements in the MUC4 promoter, and butyrate-responsive elements in the MUC5B promoter. In conclusion, MUCs exhibited distinct expression patterns in the gut. Their expression was disrupted in UC, regardless of the treatment protocols. Abnormal MUC1, MUC4, and MUC5B expression marked the barrier dysfunction in UC. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Inflammatory Bowel Disease)
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19 pages, 3822 KiB  
Article
Phytocannabinoids Reduce Inflammation of Primed Macrophages and Enteric Glial Cells: An In Vitro Study
by Gal Cohen, Ofer Gover and Betty Schwartz
Int. J. Mol. Sci. 2023, 24(19), 14628; https://doi.org/10.3390/ijms241914628 - 27 Sep 2023
Cited by 1 | Viewed by 1282
Abstract
Intestinal inflammation is mediated by a subset of cells populating the intestine, such as enteric glial cells (EGC) and macrophages. Different studies indicate that phytocannabinoids could play a possible role in the treatment of inflammatory bowel disease (IBD) by relieving the symptoms involved [...] Read more.
Intestinal inflammation is mediated by a subset of cells populating the intestine, such as enteric glial cells (EGC) and macrophages. Different studies indicate that phytocannabinoids could play a possible role in the treatment of inflammatory bowel disease (IBD) by relieving the symptoms involved in the disease. Phytocannabinoids act through the endocannabinoid system, which is distributed throughout the mammalian body in the cells of the immune system and in the intestinal cells. Our in vitro study analyzed the putative anti-inflammatory effect of nine selected pure cannabinoids in J774A1 macrophage cells and EGCs triggered to undergo inflammation with lipopolysaccharide (LPS). The anti-inflammatory effect of several phytocannabinoids was measured by their ability to reduce TNFα transcription and translation in J774A1 macrophages and to diminish S100B and GFAP secretion and transcription in EGCs. Our results demonstrate that THC at the lower concentrations tested exerted the most effective anti-inflammatory effect in both J774A1 macrophages and EGCs compared to the other phytocannabinoids tested herein. We then performed RNA-seq analysis of EGCs exposed to LPS in the presence or absence of THC or THC-COOH. Transcriptomic analysis of these EGCs revealed 23 differentially expressed genes (DEG) compared to the treatment with only LPS. Pretreatment with THC resulted in 26 DEG, and pretreatment with THC-COOH resulted in 25 DEG. To evaluate which biological pathways were affected by the different phytocannabinoid treatments, we used the Ingenuity platform. We show that THC treatment affects the mTOR and RAR signaling pathway, while THC-COOH mainly affects the IL6 signaling pathway. Full article
(This article belongs to the Special Issue Molecular Diagnosis and Treatment of Inflammatory Bowel Disease)
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