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Introduction

Systemic sclerosis (SSc) is a rare autoimmune disease marked by multisystemic fibrotic and vascular involvement, mainly affecting the skin, lungs, and upper digestive tract. Skin involvement may serve as a marker for visceral severity, particularly regarding pulmonary and upper digestive manifestations. This study examined its correlation with these systemic complications in SSc patients.

Aims & Methods

A retrospective, descriptive, bicentric study was conducted on SSc patients followed in the internal medicine department between 2004 and 2024. Clinical evaluation included cutaneous involvement via modified Rodnan score, pulmonary assessment by clinical examination, imaging, and pulmonary function tests. Upper digestive involvement was explored through symptoms, esophagogastroduodenoscopy, and esophageal manometry performed in the gastroenterology department to assess motility and mucosal integrity. Statistical analysis (descriptive and analytical) was performed using SPSS (version 26) with the Chi-square test and a significance threshold of p <0.05.

Results

A total of 160 patients were included, mostly female (91.2%), with a median age of 50 years (range:13–81). Localized scleroderma was diagnosed in 76.2%. Skin involvement was assessed in 121 patients using the Rodnan score (mean:15.31; range:0–51), categorized as mild (0–10) in 35%, moderate (11–20) in 15%, severe (21–30) in 16.3%, and very severe (>30) in 9.4%.
Upper digestive involvement was observed in 31.4%, 14.9%, 18.2%, and 9.1% of patients with mild to very severe skin involvement, respectively. Among associated symptoms: epigastric pain was present in 8.4%, 5%, 5%, and 3.4%; gastroesophageal reflux disease (GERD) in 21.2%, 9.3%, 16.9%, and 8.5%; and dysphagia in 15.3%, 7.6%, 13.6%, and 6.8%, respectively.
Esophageal manometry was performed in 36.2%, showing lower esophageal sphincter (LES) hypotonia in 5%, 2.5%, 5%, and 3.3% of mild to very severe cases, respectively. Aperistalsis was noted in 3.3%, 1.7%, 0.8%, and 0.8%, with rare ineffective motility and hypocontractility. No significant association was found between skin severity and upper digestive involvement, either clinically (p=0.458) or manometrically (p=0.98).
Similarly, no correlation was found between skin and pulmonary involvement. Lung disease was observed in 56.3% of localized and 19.4% of diffuse forms. Among these, interstitial lung disease was present in 26.3%, 12.7%, 16.1%, and 9.3%; pulmonary fibrosis in 15.6%, 6.4%, 8.3%, and 1.8%; and restrictive syndrome in 15%, 9.3%, 13.1%, and 5.6%, across increasing skin severity (all p >0.3).
However, pulmonary involvement was noted in 60% of patients with upper digestive symptoms. Dyspnea was reported in 66.9%, crackles in 29.4%, cough in 27.5%, and chest pain in 6.3%. Radiology showed interstitial lung disease in 58.8% and pulmonary fibrosis in 28.8%. Among these, GERD was present in 46.5%, dysphagia in 36.1%, epigastric pain in 19.2%, and isolated abdominal pain in one case. Manometry revealed LES hypotonia in 13.1%, aperistalsis in 5%, and ineffective motility in 0.6%. In contrast to skin involvement, a significant association was found between pulmonary and upper digestive manifestations (p<0.01).

Conclusion

No correlation was found between the severity of cutaneous involvement and digestive disorders. However, a significant link was observed between pulmonary involvement and upper digestive symptoms, suggesting that uncontrolled acid reflux may contribute to pulmonary fibrosis in SSc patients. This highlights the need for early management and multidisciplinary monitoring.

CORRELATION BETWEEN CUTANEOUS, PULMONARY, AND UPPER DIGESTIVE INVOLVEMENT IN SYSTEMIC SCLEROSIS

Sarra Laabidi 1, Faten GHRAB 1, Tayssir Ben Achour 1, DONIA GOUIAA 1, sahar chtioui 1, lilia zouiten 1, BEN MUTAPHA EP BEN ZID Nadia 1, Meriem Serghini Ep Ghachem 1, Asma Labidi 1, Monia Fekih 1

1 La Rabta Hospital, Tunis, Tunisia

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

OESOPHAGEAL, GASTRIC AND DUODENAL (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Nurse Programme (Complete Session)

Event

UEG Week Berlin 2025

Session

IBD nurses: All around the gut

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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PRECISION-CUT INTESTINAL SLICES PROVIDE EX VIVO ASSESSMENT OF REGION-SPECIFIC IMMUNE RESPONSES AND EFFICACY OF FILGOTINIB IN CROHN'S DISEASE

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Introduction

Inflammatory bowel disease (IBD) is a growing global health problem with increasing prevalence. Current therapeutic strategies for IBD are mainly aimed at modulating the dysregulated immune activity in the intestinal mucosa. Targeting the JAK/STAT signalling pathway has been shown to be highly effective in ulcerative colitis, but not in Crohn's disease (CD), where efficacy was found to be insufficient in the initiation phase of a clinical trial [1]. Failure of the therapeutic response in Crohn’s disease may be influenced by the unique immune microenvironments in the small and large intestine and their characteristic cytokine profiles and immune cell compositions.

Aims & Methods

To gain deeper insight into region-specific efficacy in the inflamed ileum versus colon, this study investigates the immunomodulatory effects of filgotinib, a Jak1 inhibitor, using precision-cut intestinal slices (PCIS) from patients with Crohn's diseases. PCIS are viable, ultra-thin human tissue slices that retain the original intestinal architecture ex vivo and contain important cell types, including resident immune cells.
PCIS were prepared from resected ileal and colonic tissue of CD patients. The slices were cultured ex vivo and stimulated with concanavalin A or anti-CD3/CD28 antibodies to induce T cell-driven inflammatory responses. Filgotinib (1-100 µM) was applied to assess the immunomodulatory effects of JAK1 inhibition following Concanavalin A preactivation. To exclude treatment-related toxicity, cellular integrity was evaluated using an LDH release assay. Tissue morphology was examined by H&E staining and immunofluorescence. The immune response was assessed by multiplex ELISA of 20 cytokines.

Results

After filgotinib treatment, primary tissue slices from the ileum and colon of CD patients remained viable. Regional morphological characteristics of ileum and colon tissue were preserved after ex vivo cultivation, with prominent villi and smaller crypts in the ileum, and larger, more frequent crypts and flattened villi in the colon. Compared to non-CD tissue slices, Crohn’s disease-related changes, such as immune cell accumulation, were also observed in CD tissue slices ex vivo. Upon T cell-specific stimulation with anti-CD3/CD28 antibodies, region-specific immune reactivity was observed. Colonic PCIS showed an increased release of IL-2 (~3-fold), IL-10 (~2‑fold) and TRAIL (~4-fold) compared to ileal PCIS, indicating a stronger involvement of Th and regulatory T cells in the colon. In contrast, ileal PCIS showed higher levels of MIP-3α (2-fold) and granzyme A (~8-fold) after stimulation, suggesting increased cytotoxic T cell activity in this region. Filgotinib treatment showed region-specific differences in its ability to modulate cytokine release in PCIS of CD patients. In colonic PCIS, filgotinib reduced the induced secretion of Th17-associated cytokines such as IL-17F and IL-22 by up to 95%, whereas in ileal PCIS it showed no effect on the same cytokines.

Conclusion

In conclusion, filgotinib exhibited more potent anti‑inflammatory effect on Th17 cells in the colon, and a markedly reduced efficacy in the ileum. This study demonstrates for the first time that precision-cut intestinal slices can be used to predict region-specific drug response in inflamed intestinal tissue ex vivo, underscoring the critical importance of region-specific immune profiling in IBD and highlight the limited efficacy of JAK1 inhibition in ileum. This ex vivo, patient-derived model represents a valuable platform for evaluating localised treatment efficacy and advancing personalised therapeutic strategies in IBD.

References

[1] Rogler G. Efficacy of JAK inhibitors in Crohn's Disease. J Crohns Colitis. 2020 Aug 1;14(Supplement_2):S746-S754. doi: 10.1093/ecco-jcc/jjz186

PRECISION-CUT INTESTINAL SLICES PROVIDE EX VIVO ASSESSMENT OF REGION-SPECIFIC IMMUNE RESPONSES AND EFFICACY OF FILGOTINIB IN CROHN'S DISEASE

Klaudia Maria Grieger 1, Valerie Beneke 1, Vanessa Neuhaus 1, Ulf Kulik 2, Heiko Aselmann 3, Benjamin Gundert 3, Armin Braun 1, Christina Hesse 1, Susann Dehmel 1, Katherina Sewald 1

1 Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany

2 Hannover Medical school (MHH), Hannover, Germany

3 KRH Klinikum Region Hannover, Hannover, Germany

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine

Submission format

Abstract

Session

Predicting response to IBD therapy

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Accreditation for a newly recruited endoscopy nurse

Anne Vidil 1

1 None, None, France

Event

UEG Week Berlin 2025

Topics

Nurses

Session

Education: Important tool for quality in endoscopy

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Acetaminophen-induced liver failure (AILF) has a high fatality rate and limited therapeutic approaches at present. Type 1 conventional dendritic cells (cDC1) are one of the major subgroups of cDCs in the liver, which is not only an important type in initiating adaptive immune response, but also can promote the generation, stability and function of Regulatory T (T_reg) cells through various mechanisms. cDC1 maintains liver immune homeostasis by regulating the balance between immune activation and tolerance. Nevertheless, the precise involvement and mechanistic contributions of hepatic cDCs in AILF remain to be elucidated.

Aims & Methods

Multiplex Immunohistochemistry (mIHC), flow cytometry, spatial transcriptomics (ST), single-cell RNA sequencing (scRNA-seq) and intravital 3D imaging were used to characterize the distribution and frequency of the cDC1. Bulk RNA-seq, metabolomic analyses, Cleavage Under Targets and Tagmentation (CUT&Tag) and Chromatin immunoprecipitation (ChIP)-qPCR assay were employed to explore the molecular mechanisms. CD11c^creXCR1^f/f, CD11c^creIDO1^f/f, CD11c^creP300^f/fand Foxp3^DTRmice, various mouse primary cells, human liver and serum samples were applied to verify the discoveries of bioinformatics analysis. Intravenous delivery of tolerogenic dendritic cells (tolDCs) was used to elucidate their regulatory effects on T_reg cells and roles in the AILF process.

Results

Our analyses revealed that the amount of cDC1 was significantly reduced across both clinical AILF cohorts and mouse AILF models, with the magnitude of depletion exhibiting dose- and duration-dependent associations with APAP exposure. mIHC, ST, scRNA-seq and intravital 3D imaging delineated that cDC1 depletion impaired T_reg cells priming capacity, ultimately disrupting hepatic immune homeostasis and exacerbating AILF. Intravenous tolDCs injection demonstrated therapeutic efficacy by orchestrating hepatic T_reg cells infiltration, attenuating inflammatory responses, potentiating liver regeneration, and ultimately reversing AILF-associated pathological manifestations. The therapeutic effect of intravenous tolDCs administration was abolished after diphtheria toxin-mediated T_reg cells depletion in Foxp3^DTRmice. CD11c^creXCR1^f/fmice andwild-type mice clearing cDC1 with XCL1-antibody had exacerbated liver pathology. Mechanistically, EP300-mediated histone 3 lysine 27 acetylation (H3K27ac) in IDO1 promoter region enforced stable tolerogenic states of cDC1, these epigenetically programmed cDC1 subsequently initiated tryptophan catabolism, generating kynurenine metabolites that triggered both differentiation and functional maturation of T_reg cells. Both the DC-specific knockout and inhibition of EP300 could reduce the H3k27ac levels of IDO1. And the CD11c^creIDO1^f/fmice with APAP exposure had less T_reg cells recruitment and worse phenotype.

Conclusion

This study elucidated that EP300 orchestrated tolDCs differentiation via H3K27ac/IDO1 signaling axis, this epigenetic-metabolic cascade licensed tolDCs to recruit and activate T_reg cells, thereby preserving hepatic immune homeostasis while promoting hepatocyte proliferation and tissue repair. These findings highlight novel therapeutic targets for reversing AILF pathogenesis.

EP300/H3K27AC/IDO1 SIGNALING AXIS REGULATES THE CROSSTALK BETWEEN TOLDCS AND T<SUB >REG</SUB> CELLS TO PROMOTE LIVER REGENERATION IN ACETAMINOPHEN-INDUCED LIVER FAILURE

Shuai Chen 1, Ziwen Tao 1, Chang-Qing Yang 2

1 Tongji Hospital, School Of Medicine, Tongji University, Shanghai, China

2 Tongji University Tongji Hospital Dept. of Gastroenterology, Shanghai, China

Conference

UEG Week Berlin 2025

Topics

Hepatobiliary

Submission format

Abstract

Session

Liver inflammation and injury (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Acetaminophen (APAP) overdose is a primary cause of drug-induced liver injury (DILI). Although the inflammatory microenvironment plays a critical role in APAP-induced liver injury (AILI), its cellular interaction network and molecular regulatory mechanisms remain incompletely elucidated. Krüppel-like factor 4 (KLF4), a zinc finger transcription factor, is known to regulate monocyte differentiation, but its functional role in the AILI inflammatory microenvironment remains unclear. This study aims to investigate the regulatory effects of myeloid KLF4 deletion on the AILI microenvironment.

Aims & Methods

By integrating multidimensional omics analysis and a myeloid-specific Klf4 knockout mouse model, we dynamically dissected microenvironmental remodeling during AILI progression. Liver samples were collected for RNA sequencing, combined with single-cell transcriptomics, flow cytometry, and molecular interaction validation to clarify the KLF4-dependent cellular subpopulation interaction network. In vivo liver imaging, histology, biochemical assays, and molecular experiments were performed to validate KLF4-dependent intercellular interactions. Primary hepatocytes and hepatocyte cell lines were used for in vitro verification.

Results

Myeloid-specific KLF4 deletion led to an increase in CXCL2⁺CXCL3⁺CD24⁺ monocytes, which activated the NF-κB signaling pathway to secrete CXCL2/CXCL3 chemokines. These chemokines bound to the CXCR2 receptor on neutrophils, driving neutrophil infiltration and neutrophil extracellular traps (NETs) formation, while amplifying the TNF-α signaling pathway. Concurrently, myeloid KLF4 knockout induced enrichment of CXCL1⁺IL17RA⁺ endothelial cells. Neutrophil-derived NETs promoted endothelial phenotypic switching toward pro-inflammatory polarization, while endothelial-derived CXCL1 further recruited neutrophils, establishing a "monocyte-neutrophil-endothelial" cellular subpopulation interaction that perpetuated microenvironmental inflammation.

Conclusion

This study reveals the molecular mechanism by which KLF4 drives inflammatory cascades in the AILI microenvironment through regulation of the myeloid-endothelial interaction network. We propose therapeutic strategies targeting NETs formation or the CXCL2/CXCL3-CXCR2 axis, providing novel targets for precise intervention in AILI.

KLF4 ORCHESTRATES MYELOID-ENDOTHELIAL CROSSTALK VIA CXCL2/CXCL3-CXCR2 AXIS TO DRIVE NEUTROPHIL EXTRACELLULAR TRAPS AND INFLAMMATORY CASCADES IN ACETAMINOPHEN-INDUCED LIVER INJURY

Qicheng Zhuang 1, Li Chen 1, Chang-Qing Yang 2

1 Tongji University, Shanghai, China

2 Tongji University Tongji Hospital, Shanghai, China

Conference

UEG Week Berlin 2025

Topics

Hepatobiliary

Submission format

Abstract

Session

Liver inflammation and injury (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Esophageal Squamous Cell Carcinoma (ESCC) remains a significant global health problem with few therapeutic options and poor prognosis. Camrelizumab, an anti-PD-1 immune checkpoint inhibitor, has been shown in clinical trials to be of potential value in the treatment of advanced or metastatic ESCC as monotherapy or in combination with chemotherapy or anti-angiogenic therapy.

Aims & Methods

The aim of this study is to evaluate the clinical efficacy and safety profile of Camrelizumab in patients with esophageal squamous cell carcinoma, with the main outcomes being progression-free survival (PFS), objective response rate (ORR), and treatment-related adverse events.
We conducted a comprehensive search of PubMed, Scopus, Web of Science, Embase, and Cochrane from their inception to April 2025, focusing on randomized controlled trials (RCTs) and observational studies evaluating Camrelizumab for the treatment of esophageal squamous cell carcinoma. Meta-analyses utilized a random-effects model to calculate odds ratios, mean differences, and 95% confidence intervals for adverse events and total patients.

Results

Out of 1,563 studies initially screened, 15 studies met the inclusion criteria for our meta-analysis, comprising adult patients. Meta-analysis established a median progression-free survival (PFS) of 7.60 months (95% CI: 6.00–9.19). The major pathological response rate (MPR) was 0.42 (95% CI: 0.37–0.48), and the objective response rate (ORR) was 0.53 (95% CI: 0.38–0.68). The R0 resection rate was also remarkably high at 0.98 (95% CI: 0.96–1), and the disease control rate (DCR) was 0.87 (95% CI: 0.64–1). The pathological complete response rate (pCR) was 0.31 (95% CI: 0.20–0.43).
Regarding safety, the most common treatment-related adverse events were leukopenia 0.45 (95% CI: 0.23–0.68), neutropenia 0.30 (95% CI: 0.19–0.41), anemia 0.14 (95% CI: 0.03–0.29), thrombocytopenia 0.09 (95% CI: 0.03–0.17), and elevated transaminases 0.06 (95% CI: 0.02–0.12). Pneumonia 0.17 (95% CI: 0.11-0.23) and hypertension 0.12 (95% CI: 0.06-0.19) were the other immune-related adverse events. The majority of these events were tolerable and within safe parameters.

Conclusion

Camrelizumab demonstrates promising efficacy in the treatment of esophageal squamous cell carcinoma with satisfactory rates of ORR, MPR, and R0 resection. The safety profile is acceptable with controllable adverse effects. These findings support the potential therapeutic value of camrelizumab as a significant treatment strategy in multimodal treatment of esophageal squamous cell carcinoma and the need for further research to optimize its clinical use.

EFFICACY AND SAFETY OF CAMRELIZUMAB IN ESOPHAGEAL SQUAMOUS CELL CARCINOMA: A SYSTEMATIC REVIEW AND META-ANALYSIS

‪Ekram Hasanin 1, Hamza Khelifa 2

1 University Of Tripoli, Tripoli, Libya

2 Faculty of Medicine University of Oran 1 Ahmed Ben Bella, Oran, Algeria

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

OESOPHAGEAL, GASTRIC AND DUODENAL (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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