Frontiers in immunology · 2026
Saccharomyces boulardii CNCM I-745 protects against small intestinal injury in a model of gliadin-peptide-induced sterile inflammatory enteropathy.
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Lezcano Aluminé, Miculan Emanuel, Ducca Geronimo, Ruera Carolina, Iribarren María Luz, Tixador Philippe, Roux Xavier, Chirdo Fernando Gabriel
Аннотация
INTRODUCTION: Inflammation of the small intestine can be caused by infections, immune-mediated disorders (such as celiac disease) and medications, leading to malabsorption, chronic diarrhea, and subclinical alterations including increased gut permeability and systemic inflammation. It has been suggested that probiotics can restore barrier integrity and reduce inflammation. The objective of the present study was to evaluate the effects of the probiotic yeast Saccharomyces boulardii CNCM I-745 (Sb) in a mouse model of sterile, inflammation-induced enteropathy based on intragastric administration of the gliadin peptide p31-43. Challenge with this peptide induces histological changes in the small intestinal mucosa, causes an elevation in inflammatory markers, and promotes cell death.
METHODS: The mice were challenged with a single dose of p31-43 or multiple doses over a three-week period, with or without Sb coadministration. Intestinal damage was assessed with regard to histologic features, mRNA gene expression (using RT-qPCR assays), caspase-1 activation (using Western blots), and cell death (using TUNEL reaction).
RESULTS AND DISCUSSION: Compared with mice treated with single or repeated doses of p31-43 alone, concomitant Sb treatment was associated with significantly better histological parameters, with restoration of the villus-height-to-crypt-depth ratio and less intraepithelial lymphocyte infiltration. Sb prevented the p31-43-induced upregulation of Cxcl10 expression. A Western blot analysis demonstrated that Sb attenuated caspase-1 activation, which indicated the suppression of p31-43-induced inflammasome activation. Furthermore, Sb prevented the increase in cell death observed following p31-43 treatment. No differences in goblet cell numbers were observed. However, Muc2 mRNA expression was upregulated following p31-43 treatment alone or in combination with Sb. Similarly, the analysis of the expression of markers associated with epithelial cell proliferation and differentiation (Atoh1 and Hes1) suggested a potential shift toward enhanced differentiation of secretory epithelial cells. In conclusion, Saccharomyces boulardii CNCM I-745 significantly attenuated mucosal damage, inflammation, and cell death in a murine model of small intestinal inflammation. These results suggest that Sb has the potential to prevent or alleviate inflammation-induced damage to the small intestine and underscore the importance of probiotic yeasts and the mycobiome in modulating host responses in the gut. Clinical evaluation in celiac disease and related disorders is now warranted.
METHODS: The mice were challenged with a single dose of p31-43 or multiple doses over a three-week period, with or without Sb coadministration. Intestinal damage was assessed with regard to histologic features, mRNA gene expression (using RT-qPCR assays), caspase-1 activation (using Western blots), and cell death (using TUNEL reaction).
RESULTS AND DISCUSSION: Compared with mice treated with single or repeated doses of p31-43 alone, concomitant Sb treatment was associated with significantly better histological parameters, with restoration of the villus-height-to-crypt-depth ratio and less intraepithelial lymphocyte infiltration. Sb prevented the p31-43-induced upregulation of Cxcl10 expression. A Western blot analysis demonstrated that Sb attenuated caspase-1 activation, which indicated the suppression of p31-43-induced inflammasome activation. Furthermore, Sb prevented the increase in cell death observed following p31-43 treatment. No differences in goblet cell numbers were observed. However, Muc2 mRNA expression was upregulated following p31-43 treatment alone or in combination with Sb. Similarly, the analysis of the expression of markers associated with epithelial cell proliferation and differentiation (Atoh1 and Hes1) suggested a potential shift toward enhanced differentiation of secretory epithelial cells. In conclusion, Saccharomyces boulardii CNCM I-745 significantly attenuated mucosal damage, inflammation, and cell death in a murine model of small intestinal inflammation. These results suggest that Sb has the potential to prevent or alleviate inflammation-induced damage to the small intestine and underscore the importance of probiotic yeasts and the mycobiome in modulating host responses in the gut. Clinical evaluation in celiac disease and related disorders is now warranted.