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Identifying disease trajectories by AI

Florian Tran 1

Affiliations

1 University Medical Center Schleswig-holstein, Campus Kiel, Kiel, Germany

Summary

AI Generated

Machine learning algorithms can identify distinct disease trajectory patterns in IBD patients starting biologic therapy, potentially enabling prediction of treatment response and comprehensive disease control.

The speaker presented work using group-based trajectory modeling and k-means algorithms to classify IBD patients into distinct response patterns including rapid responders, slow responders, rebounders, and partial responders based on daily symptom data.
Post-hoc analysis of the filgotinib Selection study and reanalysis of vedolizumab versus adalimumab trials demonstrated that fast responders show molecular differences on RNA sequencing and are most likely to achieve comprehensive disease control as stated by the speaker.
The speaker's group analyzed 380 ulcerative colitis patients in Kiel with different biologics and reported different trajectory groups showed different rates of achieving comprehensive disease control at week 52.
The Opt IBD consortium funded by the German Ministry of Health is developing an app for daily patient symptom entry to enable machine learning-based prediction of therapy outcomes and potentially guide therapy switch decisions.
The Three TR EU-funded consortium combined phase two, three, and four registration trials from pharma partners and has recruited 600 IBD patients across six European sites to collect multi-omics data including RNA sequencing, serum samples, and microbiome data.
The speaker introduced the term minimal residual inflammatory disease and described a new European consortium to study early-disease patients in remission using wearable devices and patient diaries to predict flare-ups.

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Abstract

Event

UEG Week Berlin 2025

Topics

Histopathology IBD Nurses

Session

The art of making clinical research precise: AI – friend or foe?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Jonas Halfvarson

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Matthieu Allez

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Laurent Peyrin-Biroulet

NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

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TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Presentation

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How to handle the frail

Jonas Halfvarson 1

Affiliations

1 Örebro University, Örebro, Sweden

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Nurses Paediatrics Primary Care

Session

IBD across all ages

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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IL-23

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NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Siyan Cao

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Presentation

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… after ileocecal resection of localised Crohn's disease

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… after ileocecal resection of localised Crohn's disease

Matthieu Allez 1

Affiliations

1 Saint-Louis Hospital, AP-HP, Université Paris Cité, Paris, France

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Abstract

Event

UEG Week Berlin 2025

Topics

Colorectal IBD Surgery

Session

Predicting patient outcomes...

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Jonas Halfvarson

… after ileocecal resection of localised Crohn's disease

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Laurent Peyrin-Biroulet

NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Siyan Cao

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Presentation

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IL-23

Laurent Peyrin-Biroulet 1

Affiliations

1 Inserm NGERE and University of Lorraine, Vandœuvre-lès-Nancy, France

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine

Session

What's new in advanced therapies for IBD in 2025?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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How to handle the frail

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IL-23

Laurent Peyrin-Biroulet

NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Siyan Cao

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Presentation

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NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

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NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Kaming Ma 1, Parakkal Deepak 2, Matthew Ciorba 3, Siyan Cao 1

Affiliations

1 Washington University in St. Louis, St. Luis, United States

2 Washington University in St. Louis, St. Louis, United States

3 Matthew Ciorba, MD Professor of Medicine, Director of Inflammatory Bowel Disease Center, Waschington University in Saint Louis, Washington DC, United States

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Abstract

Introduction

Very early onset inflammatory bowel disease (VEO-IBD) is often associated with a severe disease course and unique characteristics including an underlying monogenic defect. In this study, we identified new pathogenic mutations in CGNL1 associated with VEO-IBD and other inflammatory GI disease. CGNL1 (Cingulin Like 1) encodes an epithelial junctional protein whose function was previously unknown in the gastrointestinal tract.

Aims & Methods

Whole exome sequencing (WES) was performed on the affected patient with VEO-IBD and all first-degree relatives with IBD and other inflammatory disease. Intestinal epithelial organoids (IEOs) were generated from the affected patient and were characterized by transepithelial electrical resistance (TEER), FITC-dextran permeability assay on epithelial cell monolayer, immunostaining, RNA sequencing, and transmission electron microscopy (TEM). In addition, we generated a new Cgnl1^-/- mouse model, which was characterized using FITC-dextran permeability assay, TEM, dextran-sodium sulfate (DSS)-induced colitis, and infections by Citrobacter rodentium and Clostridioides difficile. Single-cell datasets were analyzed to determine CGNL1 expression in IBD, primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH).

Results

In the affected patient with VEO-IBD who required early total colectomy and pouch formation with coexistent PSC and celiac disease, WES identified two rare, new, pathogenic variants in the CGNL1 gene. Both pathogenic variants were also present in the patient’s younger sister, who has a similar history including early-onset, fulminant ulcerative colitis requiring total colectomy with ileostomy and PSC-AIH overlap syndrome. Furthermore, multiple relatives of the patient suffer from IBD and other inflammatory conditions including celiac disease, eosinophilic esophagitis, and type-1 diabetes. The RNA and protein levels of CGNL1 were significantly diminished in the patient’s intestinal epithelial cells compared to that of healthy individuals and other IBD patients by RNA-seq, immunoblotting, and immunostaining. The patient’s IEOs from pouch body and pre-pouch ileum formed smaller 3D spheroids with altered cell composition and significantly impaired barrier function compared to those from healthy controls and other IBD patients. Immunofluorescence and TEM demonstrated that CGNL1 is required for the assembly of junctional complexes in human IEOs and an epithelial cell line. Similarly to findings from the patient, impaired junctional complexes in intestinal epithelial cells and elevated intestinal permeability were present in Cgnl1^-/- mice at steady state. Cgnl1^-/- mice showed substantial vulnerability to DSS-induced colitis and bacterial infections that directly compromise the epithelial barrier. In addition, 6-month-old Cgnl1^-/- mice exhibited spontaneous inflammation in the colon and terminal ileum due to disrupted intestinal barrier, which was microbiome-dependent. Furthermore, single-cell analysis revealed diminished expression of CGNL1 in the intestinal and hepatic epithelial cells from patients with IBD or PSC/AIH, respectively.

Conclusion

The pathogenic CGNL1 variants contribute to VEO-IBD by disrupting gut barrier integrity, as demonstrated by patient’s cells and novel murine models. This study expands our understanding of epithelial barrier impairment in the pathogenesis of VEO-IBD, and highlights intestinal epithelium as a therapeutic target in some IBD patients.

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine

Submission format

Abstract

Session

New insights into IBD pathology

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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How to handle the frail

Jonas Halfvarson

… after ileocecal resection of localised Crohn's disease

Matthieu Allez

IL-23

Laurent Peyrin-Biroulet

NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Siyan Cao

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Presentation

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TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

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TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Kyle Jackson 1, Heather Galipeau 2, Amber Hann 2, Marco Constante 2, Megan Zangara 3, Alexandra Fuentas 2, Chiko Shimbori 2, Premysl Bercik 2, Brian Coombes 3, Zeinab Hosseinidoust 1, Elena Verdu 2

Affiliations

1 McMaster University, Hamilton, Canada|||Farncombe Family Digestive Health Research Institute, Hamilton, Canada

2 Farncombe Family Digestive Health Research Institute, Hamilton, Canada

3 McMaster University, Hamilton, Canada

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Abstract

Introduction

Current therapies for inflammatory bowel disease (IBD) suppress inflammation rather than inhibiting underlying microbial drivers. Treatment failures of frontline interventions, including corticosteroids, can lead to dose escalation and risk of adverse effects.^1,2 Bacteria with pro-inflammatory potential, like adherent-invasive Escherichia coli (AIEC), have been postulated as a possible microbial driver in Crohn’s disease (CD), however, targeting these bacteria with precision in IBD remains challenging.^3,4 Most antibiotics have broad-spectrum activity and disturb the background microbiome, which may exacerbate inflammation.⁵ Attention has shifted towards bacteriophages, yet their underlying mechanisms of treating IBD, and how they may work as an adjunctive therapy, remains elusive.

Aims & Methods

We aimed to assess whether and how phage therapy, specific for a CD-associated bacterium, reduces colitis severity using gnotobiotic mouse models.
In vitro kill curves and biofilm challenges were used to identify lytic phage candidates. Adult germ-free C57BL/6 mice were colonized with altered Schaedler-flora (ASF) and E. coli NRG857c (NRG), a CD-associated isolate. After 3 weeks, mice were treated with an NRG-specific lytic phage (1x10⁹ PFU/dose; daily or TIW) or vehicle (PBS) for 2 weeks (n=6/group) and then exposed to 1 cycle of dextran sulfate sodium (2%; DSS) in drinking water. PBS-treated mice (n=6) not exposed to DSS served as controls. Phage treatment was also tested in a spontaneous model of colitis using C57BL/6NTac-Il10^em8Tac (IL-10^-/-) mice, treated weekly. Mice were monitored daily for weight, stool consistency, and occult blood. Fecal contents were cultured to determine bacterial load, and the expression of NRG fimS was quantified using qPCR as an assessment of virulence. At endpoint, colon tissues were collected for histological and immunohistochemistry analysis to quantify colitis severity and NRG infiltration, respectively. Additional C57BL/6 mice were colonized and treated as previously described. During colitis induction, mice received a low-dose of budesonide (2μg/day)⁶ (n=5) or vehicle (n=5) until endpoint. Mice were monitored daily for disease activity and colon tissues were collected for histological analysis. HPLC was used to determine active budesonide levels.

Results

HER259 was identified as a lytic phage against CD-associated AIEC NRG. In ASF and NRG colonized mice, HER259 reduced clinical symptoms (p< 0.001, p< 0.001) and histological scores (p< 0.0001, p< 0.001) in chemical induced and spontaneous colitis, respectively. A 1-log reduction in NRG bacterial load was observed in HER259-treated mice (p< 0.001). Reisolated NRG exhibited a reduced FimS ON/OFF ratio (p-value < 0.01). Immunohistochemistry revealed reduced infiltration of NRG into the lamina propria following HER259 treatment, with greater accumulation in the epithelium. HER259 treatment increased the efficacy of a sub-therapeutic dosing regimen of budesonide (p< 0.001), which was independent of microbial-based drug metabolism as determined by HPLC.

Conclusion

Our results demonstrate that lytic phage targeting a CD-associated bacterium attenuates colitis in two gnotobiotic mouse models. The intervention did not lead to complete eradication of the disease-driving agent, but instead modulated bacterial virulence mechanisms and enhanced responses to corticosteroid therapy. The data suggests that alternative mechanisms should be considered when translating phage therapy to treat IBD in clinical trials.

References

1. Yan, Y. et al. Commensal bacteria promote azathioprine therapy failure in inflammatory bowel disease via decreasing 6-mercaptopurine bioavailability. Cell Rep Med 4, 101153 (2023).
2. Nagayama, M., Gogokhia, L. & Longman, R. S. Precision microbiota therapy for IBD: premise and promise. Gut Microbes 17, 2489067 (2025).
3. Darfeuille-Michaud, A. et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology 127, 412–421 (2004).
4. A, D.-M. et al. Presence of adherent Escherichia coli strains in ileal mucosa of patients with Crohn’s disease. Gastroenterology 115, 1405–1413 (1998).
5. Nelson, R. L., Suda, K. J. & Evans, C. T. Antibiotic treatment for Clostridium difficile-associated diarrhoea in adults. Cochrane Database Syst Rev 3, (2017).
6. Bercik, P. et al. Chronic gastrointestinal inflammation induces anxiety-like behavior and alters central nervous system biochemistry in mice. Gastroenterology 139, (2010).

Event

UEG Week Berlin 2025

Topics

Gut Microbiota IBD

Submission format

Abstract

Session

New tales of the gut microbiome: From profiling to new therapies

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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How to handle the frail

Jonas Halfvarson

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Matthieu Allez

IL-23

Laurent Peyrin-Biroulet

NEW PATHOGENIC MUTATIONS IN AN EPITHELIAL JUNCTION GENE CONTRIBUTING TO VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE

Siyan Cao

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

UEG Standards and Guidelines

Position Paper

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Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

Summary

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Summary is not available for this content yet.

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Guideline

Abstract

This position paper by the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) Special Interest Group on Coeliac Disease (SIG-CD) presents an update to the 2016 recommendations concerning early diet and the risk of coeliac disease (CD). This update adheres to the policy that mandates reviewing guidelines every 5 years, particularly when new data emerge. The 2024 statements and recommendations are essentially similar to the 2016 recommendations. Breastfeeding, whether any amount, exclusive, or of any duration, does not reduce the risk of developing CD. Introducing gluten into an infant's diet at any time between completed 4 months (≥17 weeks) and 12 months of age does not affect the cumulative incidence of CD, although earlier introduction may lead to earlier seroconversion and CD. In observational studies involving cohorts with a known risk for CD, consuming a high amount of gluten compared to a low amount during weaning and in the subsequent childhood years—specifically the first 2–3 years, and even up to 5 years in some studies—was associated with an increased risk for CD. However, the specific optimal amounts of gluten consumption remain undetermined due to insufficient evidence on safe thresholds, and the impact of restricting gluten in the diet of healthy children of unknown risk for CD is unknown. Thus, any recommendation on the gluten amount is currently unjustifiable for the general population and infants with known HLA risk types. There is no specific guidance on the type of gluten-containing foods to be introduced at weaning.

Publisher

European Society for Paediatric Gastroenterology, Hepatology and Nutrition

Guideline

Position Paper

Topics

Immunology Paediatrics Small Intestine & Nutrition

Citation

J Pediatr Gastroenterol Nutr. 2024;79:438–445

Published

2024

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Elena Verdu

Early diet and the risk of coeliac disease. An update 2024 position paper by the ESPGHAN special interest group on coeliac disease

Hania Szajewska

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