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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

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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

Summary

AI Generated

Chief cell-specific CHIA deficiency induces SPEM through endoplasmic reticulum stress-mediated pyroptosis and IL-33/ST2-M2 macrophage axis activation, independent of parietal cell loss.

In CHIA knockout mice, chief cell loss with M2 macrophage infiltration and SPEM formation occurred while parietal cells remained, demonstrated by histology and single-cell sequencing.
CHIA deficiency caused endoplasmic reticulum dilation, mitochondrial membrane disruption, accumulation of ER stress markers (PERK, XBP-1, eIF2α/P-eIF2α, GRP78), and upregulation of pyroptosis markers (NLRP3, ACS, GSDMD, NEK7, Caspase1, Caspase11, IL-1β, IL-18).
CHIA deficiency activated the IL-33/IL-13 circuit and induced M2 macrophage polarization (F4/80 and CD163+ colocalized with NLRP3) at the gastric mucosal base.
CHIA over-expression in rescue mice reversed the pyroptosis, ER stress, immune remodeling, and SPEM development compared with controls.
Chief cell initial loss is sufficient to induce SPEM through the IL-33/ST2-M2 macrophage polarization axis, independent of parietal cell loss.

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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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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

Summary

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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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Who is at risk: Is it all about anticoagulants?

Franco Radaelli 1

Affiliations

1 Valduce Hospital, Como, Italy

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Abstract

Event

UEG Week Berlin 2025

Topics

Endoscopy Radiology & Imaging

Session

Crash course: Lower GI bleeding

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

JIng Li

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Ole Thorlacius-Ussing

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

MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

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MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

Luying Zhao 1, Shujing Xu 1, Shikai Qiao 1, Changqing Yang 1, JIng Li 1

Affiliations

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

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Abstract

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely related to the metabolic syndrome of chronic liver disease and its pathogenesis involves a variety of cell types of metabolic disorders and inflammatory response, however, treatment is limited. Mas is a G protein-coupled receptor highly expressed by myeloid cells. It may play a key role in regulating myeloid-associated inflammation and metabolic homeostasis in the process of MASLD. However, its specific mechanism of action in MASLD remains unclear.

Aims & Methods

This study aims to explore the regulatory mechanism of MAS in myeloid cells in the occurrence and development of MASLD. In this study, liver tissues of patients with MASLD and animal models of MASLD induced by high-fat diet (HFD) were analyzed. In this study, myeloid-specific Mas1 knockout (Lysm^creMas1^f/f) mice were constructed. Single-cell RNA sequencing and multi-omics analysis were used to explore the role and mechanism of myeloid Mas in HFD-induced MASLD mice.

Results

The study found that the expression of MAS protein on myeloid cells in the livers of MASLD patients and MASLD animal models was significantly increased. Mononuclear phagocyte system（MPs）undergo metabolic disorders in the MASLD model, with elevated glycolysis levels, increased lactic acid production, and at the same time, the expression of cellular senescence markers (such as p16 and p21) is upregulated, and the secretion of inflammatory factors is increased. Single-cell multi-omics analysis revealed that myeloid MAS1 knockout activated the FN1⁺CCR2⁺monocytes first. Pseudo-temporal analysis showed that the FN1⁺CCR2⁺ monocytes had spatiotemporal metabolic responses with the macrophages, significantly involving the activation of glycolysis and inflammatory senescence by myeloid MAS. Non-target metabolomics of MASLD patients also revealed elevated glycolytic metabolism and increased lactic acid secretion. Mass spectrometry revealed that Mas specifically bound to the key glycolytic protein pyruvate kinase M2 (PKM2) and activated the lactylation of transcription factor Spi1-K208 site mediated by PKM2. The lactylation of Spi1-K208 promoted the transcription of senescence-associated secretory phenotype (SASP) -related proteins. Myeloid Mas1 knockout inhibited the nuclear translocation of PKM2 and blocked the lactylation of Spi1, inhibiting the transcriptional initiation of SASP. Screening of over 100,000 small molecule compounds through a virtual drug library revealed that Theaflavin 3,3'-digallate (TFDG) might reduce the protein expression of Mas and PKM2, and block the binding of the MAS-PKM2 complex. We synthesized macrophage membrane to encapsulat PLGA nanoparticles loaded with TFDG (MM@NP-TFDG) and found that MM@NP-TFDG effectively reduced the expression level of Mas-PKM2 complex protein expression in the MASLD mouse model, inhibited the glycolytic - inflammatory senescence axis of FN1⁺CCR2⁺ monocytes and macrophages, and alleviated liver inflammation and tissue damage. While the lipid deposition in the liver is reduced and the fatty acid oxidation is enhanced.

Conclusion

This study reveals that myeloid MAS1 protein participates in the occurrence and development of MASLD by regulating PKM2-mediated Spi1 lactylation and reprogramming the metabolic-inflammatory senescence axis of MPs during the process of MASLD. This discovery provides new potential targets for the treatment of MASLD patients and is expected to offer new clinical treatment strategies for MASLD patients.

Disclosure

The authors declare no conflict of interest.

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Hepatobiliary Mechanisms & Personalised Medicine

Submission format

Abstract

Session

MASLD: Inflammatory mechanisms

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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The future of MASLD

Herbert Tilg 1

Affiliations

1 Innsbruck Medical University - Department of Medicine, Innsbruck Medical University; Innsbruck/AT, Innsbruck, Austria

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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

More Like This:

Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

Who is at risk: Is it all about anticoagulants?

Franco Radaelli

MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

JIng Li

The future of MASLD

Herbert Tilg

THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

Ole Thorlacius-Ussing

Whole diet interventions for IBS

Heidi Staudacher

UEG Presentation

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

THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

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THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

Sabrina Kousgaard 1, Alberte Holm Møllekær 2, Sebastian Mølvang Dall 2, Lone Larsen 3, Mads Albertsen 2, Ole Thorlacius-Ussing 4

Affiliations

1 Aalborg University Hospital, Aalborg, Denmark|||Aalborg University Hospital, Aalborg, Denmark

2 Aalborg University, Aalborg, Denmark

3 Aalborg University Hospital, Aalborg, Denmark|||Aalborg University, Copenhagen, Denmark

4 Aalborg University Hospital, Aalborg, Denmark

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Abstract

Introduction

Chronic pouchitis is a common complication following ileal pouch-anal anastomosis (IPAA), with limited effective treatment options.¹ Antibiotics remain the first-line therapy; however, in cases of chronic pouchitis, prolonged antibiotic use contributes to increased antimicrobial resistance within the ileal pouch microbiome.² Fecal microbiota transplantation (FMT) has been proposed as a means of restoring microbial balance. Nevertheless, randomized placebo-controlled trials have demonstrated that, although FMT can alter the microbiome, it does not confer clinical benefits compared to placebo.^3–5

Aims & Methods

Given the lack of efficacy of FMT using stool from healthy donors, the present study aims to characterize the microbiome of a healthy ileal pouch and to evaluate the impact of high antibiotic exposure in patients with chronic pouchitis.
In this cohort study, stool samples were collected from four groups: patients with a normally functioning IPAA, patients with chronic pouchitis, patients with ulcerative colitis, and healthy controls. Microbiome composition and antibiotic resistance genes were analyzed across these groups. Fecal samples underwent metagenomic sequencing, and metagenome-assembled genomes (MAGs) were reconstructed. For Escherichia coli MAGs, the antibiotic resistance gene (ARG) profiles and plasmid content were specifically examined.

Results

This study included 197 participants. A clear pattern emerged in the microbial composition, revealing that reduced alpha diversity is directly associated with declining gut function and clinical health. Both species richness and Shannon diversity were lowest in patients with chronic pouchitis and highest in healthy individuals, with intermediate levels observed in the other groups. Notably, the ileal pouch microbiome of many chronic pouchitis patients was dominated by E. coli. Given the potential clinical implications of high E. coli abundance, we further investigated the ARG profiles and plasmid content of E. coli MAGs. E. coli MAGs from chronic pouchitis patients exhibited a significantly higher frequency of single nucleotide polymorphisms (SNPs) associated with resistance to fluoroquinolones—an antibiotic uniformly used among this patient group—compared to MAGs from the normally functioning IPAA and healthy control cohorts. Furthermore, E. coli MAGs from chronic pouchitis patients harbored a greater number of plasmids, with an increased presence of plasmid-borne ARGs conferring resistance to antibiotics commonly administered in this group, relative to the other cohorts.

Conclusion

These findings demonstrate that the composition of the ileal pouch microbiome—both in chronic pouchitis and normally functioning IPAA—differs significantly from that of individuals with normal gut physiology. This suggests that the microbiome of a normally functioning IPAA may serve as a more appropriate baseline for comparative studies than the healthy gut microbiome. Additionally, our results indicate that antibiotic use exerts increased selective pressure on E. coli strains carrying antibiotic resistance genes, directly correlating with the types of antibiotics administered.

References

1. Hata K, Ishihara S, Nozawa H, et al. Pouchitis after ileal pouch-anal anastomosis in ulcerative colitis: Diagnosis, management, risk factors, and incidence. Dig Endosc 2017;29:26–34.
2. Shen B, Kochhar GS, Rubin DT, et al. Treatment of pouchitis, Crohn’s disease, cuffitis, and other inflammatory disorders of the pouch: consensus guidelines from the International Ileal Pouch Consortium. Lancet Gastroenterol Hepatol 2021;7:69–95.
3. Herfarth H, Barnes EL, Long MD, et al. Combined Endoscopic and Oral Fecal Microbiota Transplantation in Patients with Antibiotic-Dependent Pouchitis: Low Clinical Efficacy due to Low Donor Microbial Engraftment. Inflamm Intest Dis 2019;4:1–6.
4. Karjalainen EK, Renkonen-Sinisalo L, Satokari R, et al. Fecal Microbiota Transplantation in Chronic Pouchitis: A Randomized, Parallel, Double-Blinded Clinical Trial. Inflamm Bowel Dis 2021;27:1766–1772.
5. Kousgaard SJ, Cold F, Halkjær SI, et al. The effect of non-pooled multi-donor faecal microbiota transplantation for inducing clinical remission in patients with chronic pouchitis: Results from a multicentre randomised double-blinded placebo-controlled trial (MicroPouch). J Crohn’s Colitis 2024;18:1753–1766.

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

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MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

JIng Li

The future of MASLD

Herbert Tilg

THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

Ole Thorlacius-Ussing

Whole diet interventions for IBS

Heidi Staudacher

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.

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

Whole diet interventions for IBS

Heidi Staudacher 1

Affiliations

1 The University of Queensland, Melbourne, Australia

Summary

AI Generated

Summary is not available for this content yet.

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Neurogastroenterology & Motility Primary Care

Session

Diet and disorders of gut-brain interaction: From IBS to IBD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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The future of MASLD

Herbert Tilg

THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

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