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Introduction

Crohn’s disease (CD) poses a clinical challenge due to its unpredictable post-operative recurrence and the necessity for effective therapeutic interventions. The molecular mechanisms governing recurrence are poorly understood, although oxidative stress (OS) has been implicated in CD pathogenesis. However, its specific role in recurrence remains elusive. This study aimed to analyze the gene expression signatures regarding OS and their implications for CD recurrence using transcriptomic analysis.

Aims & Methods

Ileal mucosa samples were obtained from the prospective mutlicentrique cohort of CD patients undergoing surgery. They were collected from ileal resection margins (n = 196) at the time of surgery (M0) and in the neo-terminal ileum (n = 121) 6 months after surgery (M6) while patients were classified as in remission (Rem) or recurrence (Rec) based on the Rutgeerts score. Endoscopic recurrence was defined as a Rutgeerts score ≥i2b. Gene data sets (Affymetrix microarrays) were issued on a princeps paper*. Pathway analysis was conducted to identify significant OS pathways using the Ensemble of Gene Set Enrichment Analyses (EGSEA) method and through unsupervised signature generation (Independent Component Analysis) from M0 and M6 genes dataset. Statistical analyses were carried out to assess differential gene expression and pathway enrichment between Rem and Rec patients at M0 and M6.

Results

No significant genes were differentially expressed between Rem and Rec groups at M6 and M0. However, using EGSEA at M6, of the 1766 significant pathways, 40 were related to OS and predominantly overexpressed in the Rec group, indicating a potential association between OS resolution and pressure relief. At M0, of the 2556 significant pathways, 40 were related to OS and equally distributed between the Rem and Rec groups, and therefore did not predict recurrence at M6. Applying unsupervised signature generation, 140 signatures were identified and 8 were annotated as OS pathways. Theses OS pathways were upregulated at M6 in the Rec group and at M0 in the Rem group.

Conclusion

The study highlights the role of OS in CD progression and post-operative relapse. The significant increase in OS pathways at M6 in relapsed patients and at M0 in patients who remain in remission suggests that resolution of OS is necessary to counteract CD relapse. Further research is needed to delineate the role of oxidative stress in CD recurrence and to identify new therapeutic targets tailored to individual patient profiles.

References

*Ngollo et al. Identification of Gene Expression Profiles Associated with an Increased Risk of Post-Operative Recurrence in Crohn's Disease JCC 2022;16(8):1269-1280. doi: 10.1093/ecco-jcc/jjac021.

Disclosure

There is no conflict of interest regarding this abstract

TRANSCRIPTOMIC ANALYSIS REVEALS DIFFERENTIAL EXPRESSION OF OXIDATIVE STRESS PATHWAYS IN CROHN’S DISEASE PATIENTS

Jean Bouvet 1, Hang Phuong Pham 2, Clotilde Policar 3, Marjolaine Ngollo 4, Stephane NANCEY 5, Maria Nachury 6, Xavier Treton 7, Mathurin Fumery 8, Anthony Buisson 9, Nicolas Barnich 10, Sylvie Demignot 1, Madeleine Bezault 4, Lionel Le Bourhis 4, Remind Study group 4, Matthieu Allez 4, Philippe Seksik 11

1 Sorbonne University, Paris, France

2 Parean Biotechnologies, Saint-Malo, France

3 Ecole Normale Supérieure, PSL university, CNRS, Paris, France

4 Gastroenterology, Hopital Saint-Louis, APHP, INSERM U1160, Université Denis Diderot, Paris, France

5 Université Claude Bernard, Pierre Benite, France

6 CHRU Lille, Courbevoie Cedex, France

7 Institut des MICI, Neuilly sur Seine, France

8 Amiens University Hospital, Amiens, France

9 CHU Estaing Clermont-Ferrand, Clermont-ferrand, France

10 Université Clermont Auvergne, Clermont-Ferrand, France

11 Gastroenterology & Nutrition Department, Paris, France|||Sorbonne University, Paris, France

Conference

UEG Week Vienna 2024

Topics

IBD

Submission format

Abstract

Session

IBD (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

UEG Standards and Guidelines

Consensus

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Abstract

Background

The incidence and prevalence of inflammatory bowel disease [IBD] have increased significantly in low- and middle-income countries [LMICs] in recent decades. Managing IBD in these settings presents substantial challenges. This consensus aims to describe the epidemiology of IBD in LMICs and to highlight the key challenges in its diagnosis and treatment.

Method

The consensus-defining strategy followed the previous European Crohn’s and Colitis Organisation [ECCO] consensus guidelines [available at www.ecco-ibd.eu]. The authors reviewed the available evidence and formulated statements accordingly. Provisional ECCO statements and supporting text were drafted based on a comprehensive literature review and further refined through two voting rounds, which included external reviewers and national representatives from ECCO’s 36 member countries. The final ECCO statements, representing a consensus of at least 80% agreement among participants, were approved during an online meeting. Consensus statements should be interpreted in context with their accompanying commentary rather than in isolation and should not be used solely to guide patient management. The supporting text was finalized under the guidance of each working group leader [VP, HY, TK, AH] and subsequently integrated by the consensus leader [AE].

Results

Data on IBD epidemiology in LMICs remain limited. Public and healthcare professional awareness and timely access to early diagnostic modalities, advanced medical and surgical therapies, and specialist multidisciplinary care are key gaps in IBD care in LMICs. The complexity and chronic nature of IBD, along with the necessity for a multidisciplinary approach, pose significant challenges to adopting a holistic management strategy in LMICs.

Conclusion

There is a critical need for further studies to assess the specific needs of LMICs. Such research will help guide resource allocation and improve IBD management in these settings.

ECCO Consensus on management of Inflammatory Bowel Disease in low-and middle-income countries

Alaa El-Hussuna

Publisher

European Crohn’s and Colitis Organisation

Guideline

Consensus

Topics

IBD

Citation

Journal of Crohn's and Colitis; 2025

Published

2025

UEG Podcast Episode

Journal Podcast

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Fecal microbiota transplantation and the impact of COVID-19

Iago Rodríguez-Lago 1, Siew Chien Ng 2

1 Hospital Universitario de Galdakao, Bilbao, Spain

2 Chinese University of Hong Kong, Hong Kong

Topics

Gut Microbiota

Published

2022

UEG Mistakes In Articles

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The introduction and general use of new immunosuppressive agents, including biologic agents and small molecules, has revolutionised the therapeutic management of inflammatory bowel disease (IBD). Such immunosuppression may expose patients to opportunistic infections, which can be challenging to recognise. These infections are crucial due to their association with morbidity or mortality and the challenges regarding effective treatment. New evidence in this field and vaccination strategies for immunosuppressed IBD patients led to updated European Crohn’s and Colitis Organization (ECCO) guidelines in 2021. Here we discuss the errors to avoid when managing the risk of opportunistic infections in IBD patients. The discussion is based on evidence, whenever possible, and our clinical experience.

Mistakes in opportunistic infections and vaccinations in IBD and how to avoid them

Paul McLellan, Julien Kirchgesner

Topics

IBD

Citation

Kirchgesner J and McLellan P. Mistakes in opportunistic infections and vaccinations in IBD and how to avoid them. UEG Education 2022; 22: 26–28.

Published

2022

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Introduction

Decreased vagus nerve activity and increased inflammatory immune cells are observed in ulcerative colitis (UC) (1, 2). Due to its anti-inflammatory and protective properties, vagus nerve stimulation (VNS) has garnered attention for UC therapy (3). Non-invasive transcutaneous auricular vagus nerve stimulation (NitaVNS), devoid of the side effects associated with invasive techniques, demonstrates protective anti-inflammatory effects in our mouse UC-like model of colitis (4), although the specific cellular mechanisms remain unclear.

Aims & Methods

To evaluate the effects of NitaVNS on the distribution of granulocytes, macrophages, natural killer (NK) cells, and CD4⁺ and CD8⁺ T cells in the colon tissue, spleen, and mesenteric lymph nodes of a UC-like colitis mouse model, NitaVNS was administered to C57BL/6 male mice daily for 10 min, beginning one day before colitis induction with 5% dextran sulfate sodium for 5 days in water (the control group received regular water). This continued until the end of the study, with no stimulation in sham mice. The daily disease activity index (DAI) was evaluated along with distal macroscopic scores at the time of sacrifice. The frequencies of granulocytes (Ly6G), macrophages (F4/80), NK cells (NK1.1), CD4⁺ T cells (CD3, CD4), and CD8⁺ T cells (CD3, CD8) were analyzed in the cecum, proximal, mid and distal colon, spleen, and mesenteric lymph nodes (MLNs) using flow cytometry.

Results

NitaVNS in colitic mice significantly improved the DAI and macroscopic scores related to rectal bleeding, colon bleeding, fecal consistency loss, and shortened colon length compared to sham-stimulated colitic mice. In contrast, no changes were observed in the non-colitic mice. While NitaVNS did not alter the frequency of Ly6G⁺ cells in the cecum, mid/distal colon, and MLNs, it significantly decreased the positivity of these cells in the proximal colon and spleen of mice with colitis without affecting non-colitic mice. NitaVNS significantly decreased the frequency of F4/80⁺ cells in the mid-colon but did not influence these cells in the cecum, proximal and distal colon, spleen, or MLNs. In colitic conditions, NitaVNS significantly increased NK cell frequency in the spleen without affecting non-colitic mice. Moreover, NitaVNS did not alter the frequency of NK cells in the colon or MLNs in colitic or non-colitic mice. Additionally, NitaVNS did not induce changes in CD4⁺ and CD8⁺ T cell distribution in the colon tissue, spleen, or mesenteric lymph nodes of colitic and non-colitic mice.

Conclusion

These results suggest that NitaVNS could potentially reduce inflammation in colitic mice, locally and systemically, by decreasing the frequency of granulocytes in the colon and spleen and colonic macrophages. Additionally, NitaVNS increased the number of splenic NK cells, potentially contributing to its systemic effects. These findings indicate promising therapeutic potential for NitaVNS.

References

1. Ghia JE, Blennerhassett P, Kumar-Ondiveeran H, Verdu EF, Collins SM. The vagus nerve: a tonic inhibitory influence associated with inflammatory bowel disease in a murine model. Gastroenterology. 2006;131(4):1122-30.
2. Wiese JJ, Manna S, Kühl AA, Fascì A, Elezkurtaj S, Sonnenberg E, Bubeck M, Atreya R, Becker C, Weixler B, Siegmund B, Patankar JV, Prüß MS, Schumann M. Myenteric Plexus Immune Cell Infiltrations and Neurotransmitter Expression in Crohn's Disease and Ulcerative Colitis. J Crohns Colitis. 2024 Jan 27;18(1):121-133.
3. Verma N, Mudge JD, Kasole M, Chen RC, Blanz SL, Trevathan JK, Lovett EG, Williams JC, Ludwig KA. Auricular Vagus Neuromodulation-A Systematic Review on Quality of Evidence and Clinical Effects. Front Neurosci. 2021 Apr 30;15:664740.
4. Hesampour F, Tshikudi D, Veysel Özden A, Bernstein CN, Ghia JE. A54 The impact of non-invasive transcutaneous auricular nerve stimulation (NitaVNS) on the development of experimental colitis in mice. J Can Assoc Gastroenterol. 2023 Mar 7;6(Suppl 1):30.

Disclosure

F. Hesampour: None Declared, D. Tshikudi: None Declared, A. Veysel Özden: The employee of the company providing the stimulator, C. N. Bernstein: None Declared, J-E. Ghia: None Declared.

NON-INVASIVE TRANSCUTANEOUS AURICULAR VAGUS NERVE STIMULATION (NITAVNS) DEMONSTRATES SPATIALLY SPECIFIC REGULATION OF IMMUNE CELL DISTRIBUTION IN A PRECLINICAL MODEL OF ULCERATIVE COLITIS

Fatemeh Hesampour 1, Diane Tshikudi 1, Ali Veysel Özden 2, Charles N. Bernstein 3, Jean-Eric Ghia 4

1 University Of Manitoba, Winnipeg, Canada

2 Bahcesehir University, Istanbul, Turkey|||Vagustim, Istanbul, Turkey

3 University of Manitoba, Winnipeg, Canada|||University of Manitoba, Winnipeg, Canada

4 University Of Manitoba, Winnipeg, Canada|||University of Manitoba, Winnipeg, Canada|||University of Manitoba, Winnipeg, Canada|||Children’s Hospital Research Institute of Manitoba, Winnipeg, Canada

Conference

UEG Week Vienna 2024

Topics

IBD

Submission format

Abstract

Session

Identifying drug targets in IBD: Part 1 (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

UEG Standards and Guidelines

Clinical Practice Guideline

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MAIN RECOMMENDATIONS

ESGE recommends the combination of endoscopic ultrasound-guided tissue acquisition (EUS-TA) and endoscopic retrograde cholangiopancreatography (ERCP)-based tissue acquisition as the preferred diagnostic approach for tissue acquisition in patients with jaundice and distal extrahepatic biliary stricture in the absence of a pancreatic mass.
ESGE suggests that brushing cytology should be completed along with fluoroscopy-guided biopsies, wherever technically feasible, in patients with perihilar biliary strictures.
ESGE suggests EUS-TA for perihilar strictures when ERCP-based modalities yield insufficient results, provided that curative resection is not feasible and/or when cross-sectional imaging has shown accessible extraluminal disease.
SGE suggests using standard ERCP diagnostic modalities at index ERCP. In the case of indeterminate biliary strictures, ESGE suggests cholangioscopy-guided biopsies, in addition to standard ERCP

Diagnostic work-up of bile duct strictures: European Society of Gastrointestinal Endoscopy (ESGE) Guideline

Antonio Facciorusso

Publisher

European Society of Gastrointestinal Endoscopy

Guideline

Clinical Practice Guideline

Topics

Endoscopy

Citation

Endoscopy 2025; 57: 166-185

Published

2024

UEG Poster

Standard Poster

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Introduction

Fibrosis in Crohn´s disease (CD) is a complication of chronic inflammatory processes that may result in impaired gastrointestinal function and bowel strictures. However, exact pathomechanisms leading to intestinal fibrosis in CD are not fully understood. Since the de novo DNA methyltransferase DNMT3A is involved in cellular differentiation processes and genetic variants have been associated with increased risk for CD, we sought to characterize how DNMT3A loss might affect fibroblasts, the key mesenchymal cells involved in fibrosis.

Aims & Methods

We stably deleted Dnmt3a in 3T3 fibroblast cell line using CRISPR-Cas9 technology and subsequently selected GPF-positive clones using FACS sorting. Cell cultures were performed in cell culture plates with or without 0.2% gelatin coat. Reverse transcription quantitative PCR, western blot, and immunofluorescence were used to confirm Dnmt3a gene deletion and characterize wild-type (WT) and knockout (KO) cells. Cell adhesion was evaluated by fluorescence levels of calcein acetoxymethyl ester (CAM)-labelled cells that attached to cell culture plates after 1h of culture and subsequent wash. Collagen lattice assays in presence of proinflammatory and profibrotic stimuli served to assess fibroblast contractibility.

Results

3T3 fibroblasts lacking Dnmt3a acquire an activated myofibroblast phenotype (increased alpha-SMA expression) that also overexpress tissue remodeling matrix metalloproteinase Mmp3, and the inflammation-induced necroptosis marker RIPK3 when compared to their WT counterparts. In addition, Dnmt3a-depleted 3T3 cells adhere more strongly to cell culture plates. In presence of transforming growth factor (TGF)-beta, cells embedded in a 3D collagen matrix and lacking Dnmt3a build an interconnected cellular network and contract up to a 77.78% (compared to interconnected cells that reach up to 13.73% contraction by WT cells). This contraction was independent of the presence of interleukin (IL)-11. Profibrotic factors such as bleomycin prevent intercellular network formation in both WT and KO cells; hence, incapacitating cells to contract the collagen matrix.

Conclusion

We conclude that Dnmt3a is crucial for fibroblast homeostasis, including cell activation and functionality. Furthermore, TGF-beta induces higher fibroblast contractibility when Dnmt3a is lacking. Thus, additional characterization of Dnmt3a depletion in fibroblasts will deepen the understanding of fibrosis and may point towards new therapeutic approaches for this untreatable complication.

References

1. Hampe J, Franke A, Rosenstiel P, et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet. 2007;39(2):207-211. doi:10.1038/ng1954
2. Fazio A, Bordoni D, Kuiper JWP, et al. DNA methyltransferase 3A controls intestinal epithelial barrier function and regeneration in the colon. Nat Commun. 2022;13(1):6266. doi:10.1038/s41467-022-33844-2

Disclosure

The authors have no disclosures.

LACK OF DNA METHYLTRANSFERASE DNMT3A IN FIBROBLASTS IMPAIRS CELL GROWTH AND WOUND HEALING

Celia Escudero-Hernández 1, Emely Hübner 1, Sara Núñez-Torvisco 1, Antonio Rodríguez-Peña 1, Julia Montague 1, Philip Rosenstiel 2

1 University Hospital Schleswig-Holstein / Institute of Clinical Molecular Biology (IKMB), Kiel, Germany

2 Kiel University, University Hospital Schleswig-Holstein, Kiel, Germany

Conference

UEG Week Vienna 2024

Topics

IBD

Submission format

Abstract

Session

IBD (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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