# The probiotic yeast Saccharomyces boulardii CNCM I-745 prevents autophagy in macrophages and epithelial cells infected with Vibrio parahaemolyticus

## TL;DR

A probiotic yeast prevents cell damage and autophagy caused by a marine bacterium in epithelial and immune cells.

## Contribution

The study shows that S. boulardii CNCM I-745 prevents Vibrio parahaemolyticus-induced autophagy and cytotoxicity in epithelial and macrophage-like cells.

## Key findings

- Pretreatment with S. boulardii reduces intracellular Vibrio parahaemolyticus and cell damage in epithelial cells.
- S. boulardii treatment lowers autophagy and kinase activation in Vibrio-infected cells.
- Probiotic yeast downregulates JNK and p38 phosphorylation in epithelial and macrophage-like cells.

## Abstract

Although some pathogens neutralize autophagy to replicate within host cells, others exploit autophagy to induce cell death and lysis and thus acquire nutrients or escape the immune response. Vibrio parahaemolyticus (Vp, a marine bacterium that can infect humans) exerts cytotoxicity by inducing autophagy; this is followed by cell rounding and cell lysis. The probiotic yeast strain Saccharomyces boulardii CNCM I-745 (S. boulardii) has been shown to prevent infection by enteropathogenic bacteria. Here, we investigated the in vitro effects of S. boulardii on cytotoxicity and autophagy induced by Vp infection of two epithelial cell lines (HeLa and T84) and macrophage-like cells (RAW264.7). To that end, Vp-infected cells were exposed to S. boulardii cotreatment or pretreatment regimens. Pretreatment with S. boulardii of epithelial cells before infection by Vp was associated with a lower number of live intracellular bacteria, less Vp-induced morphological changes, and lower release of lactate dehydrogenase from infected cells. Importantly treatment with S. boulardii were associated with a lower degree of autophagy in Vp-infected epithelial cells and macrophage-like cells. Pretreatment and cotreatment with S.boulardii of epithelial cells downregulated the phosphorylation of the mitogen-activated kinases ERK1/2, JNK and p38 induced by Vp infection. In RAW264.7 cells, Vp infection induced the activation of JNK and p38 but only JNK phosphorylation was downregulated by S. boulardii. Taken as a whole, our data indicate that S.boulardii exerts an anticytotoxic effect on epithelial cells and prevents the Vp-induced autophagy of epithelial cells and macrophage-like cells. Our results suggest that the administration of probiotic S.boulardii CNCM I-745 could help to mitigate the effects of food-associated Vp infections.