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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

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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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UEG Standards and Guidelines

Clinical Practice Guideline

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Joint ESPGHAN/NASPGHAN Guidelines on Childhood Eosinophilic Gastrointestinal Disorders Beyond Eosinophilic Esophagitis

Alexandra Papadopoulou

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Guideline

Abstract

Introduction

Eosinophilic gastrointestinal disorders beyond eosinophilic esophagitis (non-EoE EGIDs) are rare chronic inflammatory disorders of the gastrointestinal (GI) tract. Diagnosis is based on clinical symptoms and histologic findings of eosinophilic inflammation after exclusion of a secondary cause or systemic disease. Currently, no guidelines exist for the evaluation of non-EoE EGIDs. Therefore, the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) formed a task force group to provide consensus guidelines for childhood non-EoE EGIDs.

Methods

The working group was composed of pediatric gastroenterologists, adult gastroenterologists, allergists/immunologists, and pathologists. An extensive electronic literature search of the MEDLINE, EMBASE, and Cochrane databases was conducted up to February 2022. General methodology was used in the formulation of recommendations according to the Appraisal of Guidelines for Research and Evaluation (AGREE) II and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to meet current standards of evidence assessment.

Results

The guidelines provide information on the current concept of non-EoE EGIDs, disease pathogenesis, epidemiology, clinical manifestations, diagnostic and disease surveillance procedures, and current treatment options. Thirty-four statements based on available evidence and 41 recommendations based on expert opinion and best clinical practices were developed.

Conclusion

Non-EoE EGIDs literature is limited in scope and depth, making clear recommendations difficult. These consensus-based clinical practice guidelines are intended to assist clinicians caring for children affected by non-EoE EGIDs and to facilitate high-quality randomized controlled trials of various treatment modalities using standardized, uniform disease definitions.

Publisher

European Society for Paediatric Gastroenterology, Hepatology and Nutrition

Guideline

Clinical Practice Guideline

Topics

Immunology Paediatrics

Citation

J Pediatr Gastroenterol Nutr 2024; 78: 122–152

Published

2024

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Prateek Sharma

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Federico Biagi

UEG Presentation

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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Tamara Matysiak-Budnik

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Alexandra Papadopoulou

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JIng Li

GLPs: What should gastroenterologists know about them?

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Irene Venturini

Approaching the design of low prevalence diseases

Federico Biagi

UEG Presentation

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

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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Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

Joint ESPGHAN/NASPGHAN Guidelines on Childhood Eosinophilic Gastrointestinal Disorders Beyond Eosinophilic Esophagitis

Alexandra Papadopoulou

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JIng Li

GLPs: What should gastroenterologists know about them?

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Federico Biagi

UEG Presentation

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

GUT MICROBIOTA MODULATION AS A NOVEL THERAPEUTIC APPROACH FOR IMMUNE-CHECKPOINT INHIBITORS-RELATED DIARRHEA AND COLITIS

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GUT MICROBIOTA MODULATION AS A NOVEL THERAPEUTIC APPROACH FOR IMMUNE-CHECKPOINT INHIBITORS-RELATED DIARRHEA AND COLITIS

Serena Porcari 1, Franziska Deutschbein 1, William Fusco 1, Andrea Severino 1, Debora Rondinella 1, Irene Venturini 1, Antonio Di Sabatino 2, Marco Vincenzo Lenti 2, Ettore D'Argento 1, Emilio Bria 1, Giovanni Schinzari 1, Eleonora Palluzzi 1, Olga Martelli 1, Mariagrazia Distefano 1, Carolina Maria Sassu 1, Serena Maria Boccia 1, Laura Vertechy 1, Ida Paris 1, Roberto Iacovelli 1, Chiara Ciccarese 1, Francesca Romana Ponziani 1, Claudia Marchetti 3, Giampaolo Tortora 1, Antonio Gasbarrini 1, Giovanni Cammarota 1, Gianluca Ianiro 1

Affiliations

1 Fondazione Policlinico Universitario 'A.Gemelli' - IRCCS, Roma, Italy

2 IRCCS Policlinico S. Matteo, Pavia, Italy

3 Fondazione Policlinico Universitario 'A.Gemelli' - IRCCS, Roma, Italy|||Università Cattolica del Sacro cuore, Roma, Italy

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Abstract

Introduction

Immune checkpoint inhibitors (ICIs) have marked a breakthrough in the management of a wide range of cancer types, leading to increased overall survival. However, this treatment is frequently associated with the onset of various immune-related adverse events (irAEs), including ICI-related diarrhea and colitis.¹ Current recommendations for patients with diarrhea or colitis grade 2 or higher (graded via CTCAE)² include the discontinuation of ICI and administration of immune suppressants (e.g. steroids or biologics), which may lead to worse outcomes in these patients.³Therefore, alternative therapeutic strategies to manage irAEs are needed. The gut microbiota plays a pivotal role in the onset of gastrointestinal irAEs, but the role of its therapeutic modulation on these disorders is mostly unknown. ^4,5

Aims & Methods

Our aim was to evaluate the efficacy and safety of therapeutic microbiome modulation for gastrointestinal irAEs in cancer patients. We enrolled cancer patients affected by ICI-related diarrhea/colitis referred to our Microbiome Clinic from January 2023 to March 2025. After clinical evaluation, patients were stratified according to severity of diarrhea (graded via CTCAE)² and then received a microbiome-modulating therapy. Patients were followed-up for at least 8 week after the initiation of therapy. We collected data about patient demographics (age and gender), patient’s overall health status as assessed by the the Charlson Comorbidity Index (CCI)⁶, type of cancer, oncological therapy and its suspension, time in weeks from initiation of cancer therapy to onset of diarrhea, severity of diarrhea (graded via CTCAE)², time in weeks until resolution of diarrhea and resumption of oncological therapy

Results

We enrolled 42 patients in the study period (8 males, 34 females, mean age 58,3 years-old, mean CCI-index 5.8). All patients were treated with ICI (Pembrolizumab: n=25 , Dostarlimab: n=4, Nivolumab: n=4; Atezolizumab: n=3; Novulumab and Ipilumab: n=2, Cemiplimab: n=2; Mogamulizumab: n=1; Pertuzumab: n=1). Ten patients experienced G1 diarrhea (23,8%), 16 (38,1) G2, 15 (35,7%) G3 and one G4 (2,4%). As indicated by current European Guidelines³, 30 patients (71,4%) had to interrupt ICI due to diarrhea. Multi-strain probiotics were administered to 27 (64.3% ) patients, rifaximin to 22 (52,4%). Overall, 21 patients (50%) needed therapy with systemic steroids. Seven patients who experienced ICI-related colitis refractory to steroids and biologics were successfully treated with FMT. Twenty-eight patients (66.7% ) had a resolution of the diarrhea (G0) and 11 patients (26.2%) had diarrhea G1 at a mean time of 8 weeks. Upon resolution of diarrhea, nine of the 30 patients who had interrupted ICI (30%) were able to resume the treatment. None of the patients experienced any adverse event related to gut microbiota modulation as defined by CTCAE².

Conclusion

Therapeutic modulation of gut microbiota appears to be a promising safe and effective approach for treating ICI-related diarrhea and colitis. However, these preliminary findings need confirmation through more consolidated and well-designed studies.

References

1. Dougan M, Wang Y, Rubio-Tapia A, Lim JK. AGA Clinical Practice Update on Diagnosis and Management of Immune Checkpoint Inhibitor Colitis and Hepatitis: Expert Review. Gastroenterology. 2021;160(4):1384-1393. doi:10.1053/j.gastro.2020.08.063
2. Freites-Martinez A, Santana N, Arias-Santiago S, Viera A. Using the Common Terminology Criteria for Adverse Events (CTCAE - Version 5.0) to Evaluate the Severity of Adverse Events of Anticancer Therapies. Actas Dermosifiliogr. 2021;112(1):90-92. doi:10.1016/j.ad.2019.05.009
3. Haanen J, Obeid M, Spain L, et al. Management of toxicities from immunotherapy: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol. 2022;33(12):1217-1238. doi:10.1016/j.annonc.2022.10.001
4. Wang Y, Wiesnoski DH, Helmink BA, et al. Fecal microbiota transplantation for refractory immune checkpoint inhibitor-associated colitis. Nat Med. 2018;24(12):1804-1808. doi:10.1038/s41591-018-0238-9
5. Wang T, Zheng N, Luo Q, et al. Probiotics Lactobacillus reuteri Abrogates Immune Checkpoint Blockade-Associated Colitis by Inhibiting Group 3 Innate Lymphoid Cells. Front Immunol. 2019;10. doi:10.3389/fimmu.2019.01235
6. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: Development and validation. J Chronic Dis. 1987;40(5):373-383. doi:10.1016/0021-9681(87)90171-8

Disclosure

G.I. has received personal fees for acting as speaker for Biocodex, Danone, Sofar, Malesci, Metagenics and Tillotts Pharma, and for acting as consultant and/or advisor for Ferring Therapeutics, Giuliani, Malesci and Tillotts Pharma. A.G. reports personal fees for consultancy from Eisai Srl, 3PSolutions, Real Time Meeting, Fondazione Istituto Danone, SinergieSrl, Board MRGE and Sanofi SpA personal fees for acting as a speaker for Takeda SpA, AbbVie and Sandoz SpA and personal fees for acting on advisory boards for VSL3 and Eisai. G.C. has received personal fees for acting as advisor for Ferring Therapeutics. All other authors have no conflicts of interest to disclose.

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

More Like This:

Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

Joint ESPGHAN/NASPGHAN Guidelines on Childhood Eosinophilic Gastrointestinal Disorders Beyond Eosinophilic Esophagitis

Alexandra Papadopoulou

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

GLPs: What should gastroenterologists know about them?

Prateek Sharma

GUT MICROBIOTA MODULATION AS A NOVEL THERAPEUTIC APPROACH FOR IMMUNE-CHECKPOINT INHIBITORS-RELATED DIARRHEA AND COLITIS

Irene Venturini

Approaching the design of low prevalence diseases

Federico Biagi

UEG Presentation

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

Approaching the design of low prevalence diseases

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Approaching the design of low prevalence diseases

Federico Biagi 1

Affiliations

1 University of Pavia, Pavia, Italy

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Abstract

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Standards & Guidelines

Session

The art of making clinical research precise: Options for study design

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

Joint ESPGHAN/NASPGHAN Guidelines on Childhood Eosinophilic Gastrointestinal Disorders Beyond Eosinophilic Esophagitis

Alexandra Papadopoulou

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

GLPs: What should gastroenterologists know about them?

Prateek Sharma

GUT MICROBIOTA MODULATION AS A NOVEL THERAPEUTIC APPROACH FOR IMMUNE-CHECKPOINT INHIBITORS-RELATED DIARRHEA AND COLITIS

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Approaching the design of low prevalence diseases

Federico Biagi