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Which measures are important to prevent complication of IBD

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Which measures are important to prevent complication of IBD

Elena Sonnenberg 1

Affiliations

1 Charité – Universitätsmedizin Berlin, Berlin, Germany

Summary

AI Generated

The speaker reviewed strategies for comprehensive IBD care beyond medication, emphasizing that aggressive early treatment improves outcomes while requiring careful attention to vaccination, surveillance, and patient adherence.

The speaker cited the Profile trial showing that early aggressive combination therapy with infliximab and thiopurines in Crohn's disease resulted in significantly higher steroid- and surgery-free remission compared to step-up treatment, and stated this demonstrates that stringent treatment reduces surgery and hospitalizations
Combination therapy with infliximab and thiopurines was associated with higher risk of opportunistic viral and bacterial infections in data the speaker cited from 2018, highlighting the need to balance aggressive treatment against infection risk
Vaccination recommendations include yearly influenza for all IBD patients, pneumococcal to prevent pneumonia, and herpes zoster especially with JAK inhibitors, but live vaccines are contraindicated once biologics or JAK inhibitors are started
Lifestyle advice includes smoking cessation for Crohn's disease, avoiding chronic NSAID use, Mediterranean diet avoiding processed foods, stress reduction, adequate sleep, and regular moderate physical activity including yoga for fatigue
Colorectal cancer surveillance intervals depend on risk stratification, with yearly colonoscopy recommended for patients with PSC plus IBD starting at diagnosis, and every one to three years for high-risk patients with extensive disease starting eight years after diagnosis
The speaker emphasized that adherence equals disease control and recommended IBD nurses for building trust and providing patient education, recall systems for young patients transitioning from pediatric care, and empowering patients that they can lead normal lives with proper education and care

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Nurses

Session

IBD nurses: All around the gut

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

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EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

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EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Rui Zhong 1, Meng Sun 1, Jingyi Ju 1, Mengqi Luo 1, Yufang Wang 1

Affiliations

1 West China Hospital of Sichuan University, Chengdu, China

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Abstract

Introduction

As a small but important component of the intestinal microbiota, the fungal community (mycobiota) has received increasing attention for its involvement in the pathogenesis of Crohn's disease (CD)¹. In our previous study, we identified a significantly increased relative abundance of Exophiala dermatitidis (E. dermatitidis) in the gut of patients with CD, particularly those with active disease². Caspase recruitment domain family member 9 (CARD9), a key adaptor molecule in antifungal immune responses³, has also been strongly associated with CD susceptibility⁴. In this study, we aimed to explore the potential role and underlying mechanisms of E. dermatitidis in intestinal inflammation.

Aims & Methods

To evaluate the impact of E. dermatitidis on intestinal inflammation, we generated Card9-knockout (KO) (Card9^-/-) mice and constructed a dextran sulfate sodium (DSS)-induced colitis model colonized by E. dermatitidis. The underlying molecular mechanisms were investigated by a range of biochemical approaches. Flow cytometry was performed to analyze the proportions of myeloid cells, including CX3CR1⁺ macrophages, in the colonic lamina propria (LP).

Results

Compared to mice with DSS-induced colitis alone (WT-DSS group), the DSS-treated mice colonized by E. dermatitidis (WT-DSS + Ed group) showed a significant weight loss, a worsening of disease activity, a shorter length of the large intestine, and more severe intestinal inflammation characterized by increased inflammatory cell infiltration and crypt destruction in the histological examination of colon hematoxylin and eosin (H&E) staining. Card9^-/- mice were used to further investigate whether E. dermatitis-mediated inflammation was dependent on the CARD9 signaling pathway. We observed that CARD9 deficiency protected against E. dermatitidis-exacerbated colitis, as measured by a higher trend of body weight, longer colon lengths, and amelioration of disease activity in the KO-DSS + Ed group. In addition, flow cytometric analysis of the colonic lamina propria revealed a higher percentage proportion of CX3CR1+ macrophages in the WT-DSS + Ed group and a markedly reduced proportion in the KO-DSS + Ed group. Furthermore, we identified the Mincle-Syk-CARD9-nuclear factor kappa-B (NF-κB) signaling pathway as playing an important role in mediating the inflammatory immune responses to E. dermatitidis.

Conclusion

E. dermatitidis exacerbates the DSS-induced colitis in mice through the Mincle-Syk-CARD9-NF-κB pathway with the participation of CX3CR1+ macrophages, providing a novel therapeutic strategy for CD targeting specific intestinal fungi.

References

1. Sokol H, Leducq V, Aschard H, et al. Fungal microbiota dysbiosis in IBD. Gut 2017;66:1039-1048.
2. Zeng L, Feng Z, Zhuo M, et al. Fecal fungal microbiota alterations associated with clinical phenotypes in Crohn's disease in southwest China. PeerJ 2022;10:e14260.
3. Hu A, Hu Z, Zou H, et al. CARD9 in host immunity to fungal, bacterial, viral, and parasitic infections: An update. Frontiers In Microbiology 2022;13:1021837.
4. Franke A, McGovern DPB, Barrett JC, et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci. Nature Genetics 2010;42:1118-1125.

Event

UEG Week Berlin 2025

Topics

Colorectal Gut Microbiota Mechanisms & Personalised Medicine IBD

Submission format

Abstract

Session

Dissecting the microbiome in gut inflammation

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

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Which advanced therapy should you choose in patients with fistulising Crohn's disease?

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Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse 1

Affiliations

1 Amsterdam University Medical Center, Amsterdam, Netherlands

Summary

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine Surgery

Session

Focus on fistulising Crohn’s disease

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

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Who is at risk?

Matt Rutter 1

Affiliations

1 University Hospital North Tees NHS Dept. of Gastroenterology - Gastroenterology, University Hospital, Stockton-on-Tees, United Kingdom

Summary

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Abstract

Event

UEG Week Berlin 2025

Topics

Digestive Oncology Endoscopy IBD Surgery

Session

Endoscopy, cancer and IBD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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IL-23

Laurent Peyrin-Biroulet 1

Affiliations

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

Summary

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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

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Emilie Kristine Dahl 1, Jacob Wium Bjerrum 2, Katrine Risager Christensen 2, Anita Bilde Wozniak 2, Johan Fremberg Ilvemark 2, Milos Mathias Koch 3, Paul Blanche 3, Nicolai Ditzel Vad 4, Marco Donia 2, Inge Marie Svane 2, Jakob Seidelin 2

Affiliations

1 Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

2 Copenhagen University Hospital, Herlev, Denmark

3 Copenhagen University, Copenhagen, Denmark

4 Copenhagen University Hospital, North Zealand, Denmark

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Abstract

Introduction

Immune checkpoint inhibitor (ICI) mediated enterocolitis (IMC) may lead to treatment discontinuation. Corticosteroids for IMC is associated with serious side effects and might affect cancer progression in addition to preclude continued ICI treatment. We hypothesized that vedolizumab, a gut selective α4β7 integrin inhibitor, is effective as a first-line treatment and investigated whether vedolizumab reduces corticosteroid exposure and facilitate ICI resumption.

Aims & Methods

We conducted a single center, open-label, explorative phase 2 trial including patients treated with ICI who developed IMC. Patients were randomized 1:1 ratio to receive vedolizumab (300 mg) or standard treatment with corticosteroids, with infliximab used as recue therapy for corticosteroid failure. The primary outcome was cumulative corticosteroid dose at week 30. Key secondary outcomes included cumulative corticosteroid dose at week 10, corticosteroid free remission at week 10 and ICI resumption rates.

Results

Twenty-two patients received vedolizumab, and 19 patients received standard treatment. At week 10, the mean cumulative corticosteroid use was significantly lower in the vedolizumab arm (1157 mg vs. 2207 mg). By week 30, the mean corticosteroid use remained lower but not statistically significant (1378 mg vs. 2390 mg, estimated difference 1012 mg, 95% CI -229 to 2253, p=0.107), Among patients with less severe IMC, who did not need corticosteroids during screening, vedolizumab-treated patients used in average 1729 mg less corticosteroid (95% CI 631 to 2827). Corticosteroid-free remission at weeks 2 and 10 was more common with vedolizumab. Seven patients (33.3%) in the vedolizumab group resumed with ICI compared to three (16.7%) in the standard arm. In patients with severe colitis, who required upfront corticosteroid treatment, a trend towards longer hospitalization in the vedolizumab arm was observed.

Conclusion

For patients with less severe colitis, not needing corticosteroids during screening, vedolizumab may be a viable corticosteroid-sparing option, enabling faster remission and ICI resumption.

Disclosure

The study was funded by Aage og Johanne Louis-Hansens Fond, National Research grants. Takeda Pharma provided the study drug vedolizumab.

Event

UEG Week Berlin 2025

Topics

Gut Microbiota IBD Immunology Mechanisms & Personalised Medicine

Submission format

Late-Breaking Abstract

Session

Late-breaking trials in IBD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Qin Tang 1, Xueyin Chen 1, Yongjun Zhu 1, Jian Gao 1, Song He 1, Zhihang Zhou 1

Affiliations

1 The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China

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Abstract

Introduction

Liver cancer ranks as the sixth most common malignant tumor worldwide and the third leading cause of cancer-related deaths. Hepatocellular carcinoma (HCC), accounting for approximately 90% of primary liver cancers, is among the most lethal malignancies, with a mortality-to-incidence ratio as high as 0.92. Metastasis remains a pivotal determinant of HCC patient prognosis and therapeutic efficacy, making in-depth exploration of its underlying mechanisms a critical foundation for improving clinical outcomes. Ribosomes, composed of ribosomal RNA (rRNA) and ribosomal proteins (RPs), are central to protein synthesis. Emerging evidence highlights that ribosomal heterogeneity influences tumor biology through differentially regulating protein translation. However, the specific mechanisms by which ribosomal proteins contribute to HCC metastasis remain poorly characterized, underscoring a significant gap in oncological research.

Aims & Methods

We performed a screen for ribosomal genes associated with survival in HCC patients using multiple databases through a comprehensively bioinformatics analysis. We estimated the correlation between RPS8 expression and clinicopathological features of patients in HCC. We explored the biological function of RPS8 in HCC cells via lentiviral in vitro. We further assessed the tumorigenicity of RPS8 using both subcutaneous tumor formation in nude mouse and orthotopic liver tumorigenesis in NCG mouse. multi-omics were applied for exploring the mechanism of RPS8 in HCC.

Results

Comprehensive pathological evaluation of HCC clinical specimens revealed overexpression of RPS8 in tumor tissues, which exhibited significant associations with higher tumor stage, poorly differentiated histology , microvascular invasion,and reduced overall survival.Functional studies demonstrated that knockdown of RPS8 suppressed proliferation, migration, and invasion in HCC cell lines . Overexpression of RPS8 could enhance the malignant behavior of HCC cells. Moreover, RPS8 depletion reduced subcutaneous tumor volume and orthotopic liver tumor metastasis to lungs. Mechanistically, proteomic analysis and RIP-seq revealed interferon-stimulated gene 15 (ISG15) exhibited the most significant downregulation at the protein level upon RPS8 knockdown and RPS8 directly binds to ISG15 mRNA. GO and KEGG analysis indicate that RPS8 promotes HCC invasion and metastasis by modulating cell motility and migration. Among the top five differentially expressed proteins, CCDC25, a neutrophil extracellular trap (NET) repceptor, exhibited the most significant downregulation upon RPS8 knockdown. ISG15 can bind with target proteins to form ISGlation, thus preventing the ubiquitinlation. Bioinformatic predictions have identified six potential ubiquitination modification sites in CCDC25. Additionally, molecular docking analyses suggest the presence of potential ubiquitination modification sites within the binding interface between ISG15 and CCDC25. We then performed CCDC25 overexpression in RPS8-knockdown HCC cells and CCDC25 knockout in RPS8-overexpressing HCC cells. Downregulation or upregulation of CCDC25 partially reversed the oncogenic effects of RPS8 respectively, supporting CCDC25 as a critical downstream mediator of RPS8-driven HCC progression. Finally, we found that NETs from HCC patients could promote in vivo metastasis of control cells, but showed less efficacy in RPS8-knockdown cells.

Conclusion

Ribosomal protein RPS8 promotes HCC metastasis through upregulating ISG15 to stabilize NETs receptor CCDC25 protein. These findings provide a promising therapeutic strategy targeting .

References

1.Kang J, Brajanovski N, Chan KT et al. Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy. Signal Transduction and Targeted Therapy 2021; 6.
2. Larionova TD, Bastola S, Aksinina TE et al. Alternative RNA splicing modulates ribosomal composition and determines the spatial phenotype of glioblastoma cells. Nature Cell Biology 2022; 24:1541-1557.
3.Kang JA, Kim YJ, Jeon YJ. The diverse repertoire of ISG15: more intricate than initially thought. Experimental & Molecular Medicine 2022; 54:1779-1792.
4.Yang L, Liu Q, Zhang X et al. DNA of neutrophil extracellular traps promotes cancer metastasis via CCDC25. Nature 2020; 583:133-138.
5.Zhan X, Wu R, Kong XH et al. Elevated neutrophil extracellular traps by HBV‐mediated S100A9‐TLR4/RAGE‐ROS cascade facilitate the growth and metastasis of hepatocellular carcinoma. Cancer Communications 2022; 43:225-245.

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Immunology Mechanisms & Personalised Medicine

Submission format

Abstract

Session

Bench to bedside and beyond frontiers in HCC

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

Yufang Wang

Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse

Who is at risk?

Matt Rutter

IL-23

Laurent Peyrin-Biroulet

UP-FRONT VEDOLIZUMAB VERSUS CONVENTIONAL TREATMENT FOR CHECKPOINT INHIBITOR INDUCED COLITIS – VEICO: AN OPEN LABEL RANDOMIZED CLINICAL TRIAL

Jakob Seidelin

RIBOSOMAL PROTEIN RPS8 PROMOTES HEPATOCELLULAR CARCINOMA METASTASIS VIA UPREGULATING ISG15 TO STABILIZE NEUTROPHIL EXTRACELLULAR TRAP RECEPTOR CCDC25

Zhihang Zhou

UEG's educational platform for gastroenterology education bringing recordings, courses, guidelines, and more together in one place.

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