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ANTI-INFLAMMATORY EFFECTS OF SACCHAROMYCES BOULARDII CNCM I-745 IN A MOUSE MODEL OF PROXIMAL SMALL INTESTINE GLUTEN-RELATED DISEASE

Emanuel Miculan 1, Camila Stefanelli 1, Maria Luz Iribarren 1, Geronimo Ducca 1, Alumine Lezcano 1, Gisela Perez Tolosa 1, Carolina Ruera 1, Fernando Chirdo 1

Affiliations

1 Instituto de Estudios Inmunologicos y Fisiopatologicos ( IIFP)(UNLP-CONICET), La Plata, Argentina

Summary

AI Generated

Three-week pretreatment with Saccharomyces boulardii CNCM I-745 prevented mucosal damage, cell death, and inflammasome activation in a mouse model of p31-43 gliadin peptide-induced proximal small intestine inflammation.

Administration of S. boulardii at 3g/kg/day for three weeks before p31-43 challenge prevented histological damage in proximal small intestine at both 4 hours (p<0.01) and 16 hours (p<0.0003) after peptide administration in C57BL/6 mice.
S. boulardii pretreatment blocked p31-43-induced cell death as measured by TUNEL staining (p<0.005) and prevented mucosal intraepithelial lymphocyte recruitment.
Pretreatment reduced inflammasome activation by maintaining caspase-1 at basal levels (p<0.01) compared to p31-43 challenge alone.
The authors suggest these findings on S. boulardii CNCM I-745 in proximal small intestine inflammatory conditions may be of interest in celiac disease patients.

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This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

Abstract

Introduction

Saccharomyces boulardii CNCM I-745 probiotic properties have been demonstrated for decades. The exact mechanisms behind these beneficial effects are widely documented, notably anti-inflammatory properties and preservation of the intestinal barrier integrity. However most of the current knowledge was obtained from studies focusing on infectious or inflammatory colonic diseases and very little is known regarding the effects of this yeast on small intestine pathologies.
In previous work, we showed that after oral gavage of p31-43 gliadin peptide, a fragment of gluten-derived peptides that neither binds to HLA class II molecules nor induces T cell activation, is responsible for toxic effects and strong inflammatory responses in the proximal small intestine (Gomes Castro et al., 2019, Ruera C et al, 2020). In this mouse model, intragastric administration of p31-43 elicits mucosal damage in small intestinal together with the production of inflammatory mediators, inflammasome activation, and cell death.

Aims & Methods

Aim: To study the effects of S. boulardii pre-treatment on the inflammatory response in the proximal small intestine in a mouse model of sterile inflammation induced by p31-43.
Materials and methods: Seven week-old C57BL/6 mice were housed under specific pathogen-free conditions and allowed access to autoclaved food and water ad libitum. A three-weeks pretreating phase by gavage with S. boulardii CNCM I-745 (3g/kg/day) or vehicle (Phosphate-buffered saline, PBS), was performed. Then, a single dose of 20µg of p31-43 gliadin peptide (LGQQQPFPPQQPY, at > 95% purity) per mouse or PBS, was delivered by intragastric administration. Mice were euthanized 4 or 16 hours after challenge and proximal small intestine was sampled to perform different histological analysis: villus high/crypt depth (V/C) ratio, intraepithelial lymphocytes (IELs) counting, cell death by TUNEL staining. Assessment of the activation of caspase-1, a central mediator of inflammasome pathway, was performed by Western Blot on small intestinal samples. Statistics were performed using Anova Test.

Results

The evaluation of the histological changes at the proximal small intestine showed that administration of S. boulardii was able to prevent the damage induced by p31-43 for both 4h (p< 0.01) and 16h (<0.0003) after p31-43 treatment. This treatment also prevented mucosal IELs recruitment.
The assessment of cell death by TUNEL staining on sections of the small intestine showed that S. boulardii was effective to block the induction of cell death caused by p31-43 (p< 0.005).
Pretreatment with S boulardii before the p31-43 challenge reduced inflammasome activation by maintaining caspase-1 to basal levels (p<0.01).

Conclusion

Three-week phase of preconditioning with S. boulardii before the p31-43 treatment prevented intestinal macroscopic damage, the increase in IELs numbers, cell death and inflammasome activation. These findings show the beneficial effects of S. boulardii CNCM I-745 in proximal small intestine inflammatory conditions and may be of interest in celiac disease patients.

Disclosure

Nothing to declare

Conference

UEG Week Copenhagen 2023

Topics

Small Intestine & Nutrition

Submission format

Abstract

Session

PP 03 Small intestinal (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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