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WESTERNIZED DIETS EXACERBATE TUMORIGENESIS BY EXPANDING H2S-PRODUCING DESULFOVIBRIO IN MURINE MODELS OF ATF6-DRIVEN COLON CANCER

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WESTERNIZED DIETS EXACERBATE TUMORIGENESIS BY EXPANDING H2S-PRODUCING DESULFOVIBRIO IN MURINE MODELS OF ATF6-DRIVEN COLON CANCER

Isabel Keidel 1, Jagadrupa Sahoo 1, Miriam von Stern-Gwiazdowski 2, Hélène Omer 1, Tingting Zheng 1, Miriam Wimmer 2, Andreas Dunkel 2, Katja Steiger 3, Olivia Coleman 2, Melanie Schirmer 1, Dirk Haller 1

Affiliations

1 Technical University of Munich, Freising, Germany|||Technical University of Munich, Freising, Germany

2 Technical University of Munich, Freising, Germany

3 Technical University of Munich, München, Germany

Summary

AI Generated

Westernized diets induce colorectal tumorigenesis in ATF6-overexpressing mice through expansion of hydrogen sulfide-producing Desulfovibrio bacteria, and scavenging H2S with bismuth subsalicylate prevents tumor formation.

Westernized high-lard diet induced de novo tumorigenesis in monoallelic nATF6-overexpressing mice that are otherwise tumor-free, and increased tumor burden in biallelic mice.
Supplementing dietary fiber or lowering fat content failed to protect against the westernized diet-induced tumorigenic phenotype.
Metagenomic profiling of westernized diet-exposed mice identified increased relative abundance of H2S-producing Desulfovibrio species and genes related to dissimilatory sulfate reduction.
Transferring microbiota from diet-exposed mice into germ-free nATF6 mice was sufficient to trigger tumorigenesis, demonstrating microbiota-dependent transmissibility.
Supplementing westernized diets with the H2S-scavenger bismuth subsalicylate prevented tumor formation in monoallelic mice and drastically altered microbial communities.
H2S scavenging significantly reduces diet-induced colonic tumor susceptibility, demonstrating the impact of diet in shaping cancer-related microbiome alterations.

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Abstract

Introduction

The interplay of diet and the intestinal microbiome plays a key role in developing colorectal cancer (CRC), with westernization of diets, e.g., an increase in fat and sugar and a decrease in fiber content, being the main contributor. We recently demonstrated that the endoplasmic reticulum unfolded protein response (ER-UPR) effector activating transcription factor 6 (ATF6) is associated with early and late onset of CRC in patients. Furthermore, the overexpression of ATF6 observed in a subset of CRC patients is associated with the presence of certain gut bacteria. The specific expression of activated ATF6 (nATF6) in mouse intestinal epithelial cells (nATF6^IEC) induces spontaneous development of colonic tumors in a microbiota-dependent manner, highlighting the functional relevance of ATF6 as a novel oncogenic driver.

Aims & Methods

To elucidate the adverse role of dietary fat, sugar, and fiber in tumorigenesis, we exposed nATF6^IEC mice under SPF conditions to control (chow) and westernized diets for 7 weeks after weaning. Microbial and metabolite profiles were assessed through deep metagenomic sequencing and targeted/untargeted mass spectrometry (LC-MS) analysis. Microbiota transfer of diet-exposed mice into germ-free recipients was conducted to verify the microbiota-dependent transmissibility of tumor formation. Bismuth(II)subsalicylate (BSS) was used as a dietary additive to validate the impact of bacteria-produced H₂S on tumorigenesis.

Results

Westernized high lard (HL) diet, enriched in fat and sugar and depleted in fermentable fiber, increased tumor burden in biallelic nATF6^IEC mice. Unexpectedly, HL induced de novo tumorigenesis in otherwise tumor-free monoallelic nATF6^IEC mice. Surprisingly, modifying the HL diet by supplementing dietary fiber or lowering fat content failed to protect the HL-induced tumorigenic phenotype. Metabolite profiling clearly differentiated westernized from control diets and tumor bearing from control mice. Transferring microbiota from diet-exposed mice into germ-free nATF6^IEC mice was sufficient to trigger tumorigenesis. Metagenomic profiles of westernized diet-exposed mice identified an increased relative abundance of H₂S-producing Desulfovibrio species and genes related to dissimilatory sulfate reduction. Supplementing westernized diets with the H₂S-scavenger BSS resulted in a drastic change in microbial communities as well as the prevention of tumor formation in monoallelic nATF6^IECmice.

Conclusion

These results highlight the ability of westernized diets to enhance nATF6-related tumorigenesis while altering metabolite and microbial profiles. Westernized diets favor the growth of sulfate-reducing Desulfovibrionaceae, possibly resulting in increased H₂S production. H₂S scavenging significantly reduces diet-induced colonic tumor susceptibility, clearly demonstrating the impact of diet in shaping cancer-related microbiome alterations.

Event

UEG Week Berlin 2025

Topics

Digestive Oncology Gut Microbiota Immunology Mechanisms & Personalised Medicine Colorectal

Submission format

Abstract

Session

Oncobiome

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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GLPs: What should gastroenterologists know about them?

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GLPs: What should gastroenterologists know about them?

Prateek Sharma 1

Affiliations

1 University of Kansas School of Medicine Dept. of Gastroenterology, Leawood, United States of America

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Abstract

Event

UEG Week Berlin 2025

Topics

Endoscopy Mechanisms & Personalised Medicine Surgery

Session

Obesity in Pan America

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Transglutaminase inhibition in CeD

Detlef Schuppan

UEG Presentation

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Medical treatment

David Surendran Sanders 1

Affiliations

1 Royal Hallamshire Hospital - NHS Trust, Royal Hallamshire Hospital; Sheffield/GB, Sheffield, United Kingdom

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Abstract

Event

UEG Week Berlin 2025

Topics

Immunology Small Intestine & Nutrition

Session

Coeliac or non-coeliac enteropathy?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

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Exploiting the immune response in GI cancer: Next chapter

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Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik 1

Affiliations

1 CHU de Nantes IMAD, Nantes, France

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Abstract

Event

UEG Week Berlin 2025

Topics

Digestive Oncology Hepatobiliary Immunology Mechanisms & Personalised Medicine Small Intestine & Nutrition

Session

The art of making clinical research precise: What will be new in therapy in 2030?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

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Detlef Schuppan

UEG Presentation

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IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

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IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

Zaheer Nabi 1, MARAGONI RAJESH GOUD 2, Preeti Sudha 1, D. Nageshwar Reddy 1

Affiliations

1 Asian Institute of Gastroenterology, Hyderabad, India

2 Asian Institute of gastroenterology,Hyderabad, Hyderabad, India

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Abstract

Introduction

Gastric mucosal visibility is essential for high-quality upper gastrointestinal (GI) endoscopy. While simethicone and N-acetylcysteine (NAC) have been shown to improve mucosal visibility, the optimal time interval between preparation and endoscopy remains undefined.

Aims & Methods

This randomized controlled trial evaluated the effect of timing on mucosal visibility and explored the upper limit beyond which visibility begins to decline.
In this single-center, randomized controlled trial, adult patients undergoing elective upper GI endoscopy were randomized into four groups: placebo, simethicone + NAC with endoscopy performed after 10–20 minutes, 20–30 minutes, and >30 minutes. The primary outcome was the proportion of patients achieving adequate gastric mucosal visibility (GMV), defined as a score of <7 on a validated visibility scale. A pre-specified subgroup analysis of the >30 minute group was performed by stratifying patients into 20-minute intervals (31–50, 51–70, and 71–90 minutes) to assess the durability of mucosal clarity over time.

Results

Comparison	Adequate gastric mucosal visibility (%)	P
10–20 min vs 20–30 min	27% vs 62%	0.001
10–20 min vs >30 min	27% vs 67%	0.001
10–20 min vs Placebo	27% vs 2.6%	0.001
20–30 min vs >30 min	62% vs 67%	0.174
20–30 min vs Placebo	62% vs 2.6%	0.001

1,140 patients (median age 42years, 63.2% males) were included in the study. Adequate GMV was significantly higher in all preparation groups compared to placebo (p < 0.001). The 20–30 minute and >30 minute groups demonstrated the highest rates of adequate visibility (61.5% and 73.5%, respectively), both significantly superior to the 10–20 minute group (26.9%) and placebo (2.6%). In the >30 minute subgroup analysis, the 31–50 minute interval demonstrated the highest adequacy (73.5%). The 51–70 minute group showed moderate adequacy (52.1%), which was not significantly different from the 20–30 minute group (p = 0.207). However, the 71–90 minute group had reduced adequacy (43.8%) and did not differ significantly from the 10–20 minute group (p = 0.145). No adverse events were reported across study arms.

Conclusion

Endoscopy performed between 20 and 50 minutes after mucosal preparation yields optimal gastric mucosal visibility. A decline in visibility beyond 50 minutes suggests a practical upper limit for endoscopy timing following preparation. These findings support structured, time-sensitive scheduling following mucosal cleansing to enhance procedural quality.

Disclosure

None

Event

UEG Week Berlin 2025

Topics

Endoscopy Oesophagus

Submission format

Abstract

Session

Randomised controlled trials in upper GI endoscopy

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Xuemei Liu

Transglutaminase inhibition in CeD

Detlef Schuppan

UEG Presentation

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

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Shuhui Liu 1, Zhiyuan Ma 1, Bei Ji 1, SHUN YAO 1, Taolang Li 1, Biguang Tuo 1, Xuemei Liu 1

Affiliations

1 Affiliated Hospital of Zunyi Medical University, Zunyi, China

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Abstract

Introduction

Spasmolytic polypeptide expressing metaplasia (SPEM) is a cell repair lineage and is a very important phenotype of gastric mucosal injury and precancerous lesion.
Previously, parietal cells loss is considered as the first step and followed with chief cells transdiffernation to induce SPEM. But whether chief cells initial loss cause SPEM
needs to be further investigation. Acidic mammalian chitinase (CHIA) belongs to the 18 glycosidase family and is highly expressed in the chief cells. Our previous study showed that CHIA deficiency in the chief cells is the key event to induce SPME to progress to gastric cancer (Liu et al., DDW 2023 and 2024). However, the molecular role of CHIA in the development of SPEM is need further investigated.

Aims & Methods

Electron microscopy, qRT-PCR and single-cell sequencing (scRNA-seq) technology, as well as histopathological and immunofluorescence (IF) stainning with specific markers were performed in chief cells specific CHIA knockout mouse model (CHIA^rox/rox-GIF-Dre) and wild-type mice(CHIA^rox/rox), and in CHIA over - expression mice (CHIA ^rox/rox - GIF - Dre + rAAv - CHIA) and the control group (CHIA ^rox/rox - GIF - Dre + rAAv - control).

Results

Compared with CHIA^rox/rox mice, histological analysis and scRNA-seq technology data showed that loss of chief cells with increased M2 macrophage infiltration and final SPEM formation, but remaining of parietal cells in CHIA^rox/rox-GIF-Dre mice. Electron microscopy showed CHIA deficiency in mice resulted in endoplasmic reticulum was dilated and swollen, as well as the mitochondrial membrane was discontinuous of chief cells, followed with the accumulation of endoplasmic reticulum stress marker, including PERK, XBP-1, eIF2α/P-eIF2α, and GRP78, together with upregulation of pyroptosis-related marker, including NLRP3, ACS, GSDMD, NEK7, Caspase1, Caspase11, IL-1β, and IL-18, which was detected by qRT-PCR. These data indicating that target CHIA deletion caused chief cells pyroptosis. Furthermore, qRT-PCR analysis showed that CHIA deficiency caused the activation of IL33/IL-13 circuit in the mucosa of mice. Moreover, double immunofluorescence staining confirmed that upregulation and colocalization of IL-33 induced M2 macrophage polarization markers, including F4/80 and CD163⁺ with NLRP3 in the base of gastric mucosal of CHIA^rox/rox-GIF-Dre mice when compared with CHIA^rox/rox mice.Notably, CHIA^rox/rox - GIF - Dre + rAvv - CHIA mice reversed the above process compared with controls.

Conclusion

Chief cells specific CHIA deficiency resulted in endoplasmic reticulum stress mediate NLRP3 inflammasome activation to induce chief cells proptosis.
Chief cells initial loss is sufficient and the key step to activate IL-33/ST2-M2 macrophage polarization axis to induce SPEM, which is independent of parietal cells loss.

Event

UEG Week Berlin 2025

Topics

Immunology Neurogastroenterology & Motility Small Intestine & Nutrition Oesophagus Stomach & H. Pylori

Submission format

Abstract

Session

Complexity and diversity in upper GI

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Prateek Sharma

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IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

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Xuemei Liu

Transglutaminase inhibition in CeD

Detlef Schuppan

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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Transglutaminase inhibition in CeD

Detlef Schuppan 1

Affiliations

1 Medical University Mainz - Institute of Translational Immunology, Medical University Mainz ; Mainz/D, Mainz, Germany

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Abstract

Event

UEG Week Berlin 2025

Topics

Immunology Nurses Small Intestine & Nutrition

Session

What's new in coeliac disease in 2025?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Prateek Sharma

Medical treatment

David Surendran Sanders

Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

D. Nageshwar Reddy

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Transglutaminase inhibition in CeD

Detlef Schuppan