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

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. <i>Vibrio parahaemolyticus</i> (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 <i>Saccharomyces boulardii</i> CNCM I-745 (<i>S. boulardii</i>) has been shown to prevent infection by enteropathogenic bacteria. Here, we investigated the <i>in vitro</i> effects of <i>S. boulardii</i> 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 <i>S. boulardii</i> cotreatment or pretreatment regimens. Pretreatment with <i>S. boulardii</i> 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 <i>S. boulardii</i> were associated with a lower degree of autophagy in Vp-infected epithelial cells and macrophage-like cells. Pretreatment and cotreatment with <i>S.boulardii</i> 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 <i>S. boulardii</i>. Taken as a whole, our data indicate that <i>S.boulardii</i> 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 <i>S.boulardii</i> CNCM I-745 could help to mitigate the effects of food-associated Vp infections.