Intracellular Signal Triggered by Cholera Toxin in Saccharomyces boulardii and Saccharomyces cerevisiae

Abstract

As is the case for Saccharomyces boulardii, Saccharomyces cerevisiae W303 protects Fisher rats against cholera toxin (CT). The addition of glucose or dinitrophenol to cells of S. boulardii grown on a nonfermentable carbon source activated trehalase in a manner similar to that observed for S. cerevisiae. The addition of CT to the same cells also resulted in trehalase activation. Experiments performed separately on the A and B subunits of CT showed that both are necessary for activation. Similarly, the addition of CT but not of its separate subunits led to a cyclic AMP (cAMP) signal in both S. boulardii and S. cerevisiae. These data suggest that trehalase stimulation by CT probably occurred through the cAMP-mediated protein phosphorylation cascade. The requirement of CT subunit B for both the cAMP signal and trehalase activation indicates the presence of a specific receptor on the yeasts able to bind to the toxin, a situation similar to that observed for mammalian cells. This hypothesis was reinforced by experiments with 125I-labeled CT showing specific binding of the toxin to yeast cells. The adhesion of CT to a receptor on the yeast surface through the B subunit and internalization of the A subunit (necessary for the cAMP signal and trehalase activation) could be one more mechanism explaining protection against the toxin observed for rats treated with yeasts.

Microbiota and their role in the pathogenesis of oral mucositis

“…Teeth, gingival sulcus, gingiva, tongue, cheek, lip, hard and soft palate are all microbial habitats that are colonized by distinct microbial communities which form biofilms of different complexities (Mager et al, 2003;Aas et al, 2005). Those biofilms protect the host against pathogens through mechanisms such as competition for nutrients (Momose et al, 2008) or adhesion receptors (Servin and Coconnier, 2003), production of inhibitory metabolites or anti-microbial agents against pathogens (Servin, 2004), modulation of toxin production or action (Czerucka et al, 1994;Brandão et al, 1998), and modifying inflammatory responses (Starling and Balish, 1981;Mitsuyama et al, 1986;Ohkubo et al, 1990;Clarke et al, 2010;Fagundes et al, 2012).…”

Occurrence and taxonomic characteristics of strains of predominant in African indigenous fermented foods and beverages

“…For the latter the e¡ect has been shown to be due to a reduction in the binding of C. di⁄cile toxins A and B by inhibition of toxin^receptor binding, probably due to secretion of a protease that digests both the toxins and the intestinal receptor for these toxins [68]. Also Saccharomyces yeasts have been found to protect against cholera toxin probably by adhesion of the toxin to receptors on the yeast surface [69]. Furthermore, Saccharomyces yeasts have been observed to modulate the host immune response by stimulating sIgA production and the phagocytic system in mice [70].…”

The antagonistic effect ofSaccharomyces boulardiionCandida albicansfilamentation, adhesion and biofilm formation

“…Saccharomyces boulardii is a nonpathogenic, thermophilic yeast that has been shown to be effective against a number of bacteria-induced gastrointestinal diseases (McFarland et al, 1994;Bleichner et al, 1997;Surawicz et al, 2000;Marteau et al, 2001;Czerucka & Rampal, 2002). The activity of S. boulardii against enteric bacteria involves many different mechanisms: competition with pathogens for nutrients; binding of cholera toxin to the S. boulardii cell wall, resulting in its elimination with yeast cells by peristalsis (Dias et al, 1995;Brandao et al, 1998); inhibition of pathogen adhesion; degradation of bacterial toxins and their receptors on the host mucosa (Castagliuolo et al, 1999); stimulation of the enzymatic activity and intestinal mucosa immune response; and modulation of host cell signaling and proinflammatory gene expression (Czerucka et al, 2000;Qamar et al, 2001;Sougioultzis et al, 2006). Additionally S. boulardii stimulates intestinal mucosa by secreting trophic factors and polyamines (Buts & de Keyser, 2006), contributing to the increase in host immune defense.…”