Table 2.

Mechanisms of action of Saccharomyces boulardii in specific infections.

Action of Saccharomyces boulardii	References
Clostridium difficile infection
1) Inhibits toxin A-mediated diarrhea, intestinal inflammation and histological damage by reducing toxin A-receptor binding	[Castagliuolo et al. 1996; Pothoulakis et al. 1993]
2) Releases a protease that cleaves C. difficile toxins and toxin intestinal receptors	[Castagliuolo et al. 1996; Pothoulakis et al. 1993]
3) Stimulates specific intestinal antitoxin A immunoglobulin levels	[Castagliuolo et al. 1996, 1999; Pothoulakis et al. 1993]
4) Inhibits IL-8 production and activation of the MAP kinases Erk1/2 and JNK/SAPK induced by C. difficile toxin A in human colonocytes	[Chen et al. 2006; Qamar et al. 2001]
5) Significantly fewer animals challenged with C. difficile died if given S. boulardii compared with controls	[Castex et al. 1990; Elmer and Corthier, 1991; Rodrigues et al. 1996; Toothaker and Elmer, 1984]
Helicobacter pylori infection
Alters the structure of H. pylori	[Vandenplas et al. 2009]
Vibrio cholerae infection
1) Inhibits the effect of V. cholerae toxin and hydroelectrolytic secretions by reducing cAMP activity	[Vidon et al. 1986; Czerucka et al. 1994]
2) S. boulardii and the mammalian CT receptors could be structurally and functionally similar and the yeast binds CT	[Brandao et al. 1998; Czerucka et al. 1994]
Amebic dysentery
1) Reduces the number of red cells adhering to amoebae	[Rigothier et al. 1994]
2) Decreases the number of amoebae bearing red cells	[Rigothier et al. 1994]
Infection with EHEC
1) S. boulardii modifies host signaling such as NF-κB-associated pathways activated by bacterial invasion with EHEC	[Dahan et al. 2002, 2003]
2) Addition to T84 colonocyte monolayers diminishes MLC phosphorylation and decreases transepithelial resistance in response to EHEC	[Dahan et al. 2002, 2003]
Infection with EPEC
1) Modifies EPEC infection and acts as a receptor decoy for EPEC	[Buts et al. 2006; Canil et al. 1993; Czerucka et al. 2000; Gedek, 1999b]
2) Reduces the number of intracellular EPEC	[Buts et al. 2006; Canil et al. 1993; Czerucka et al. 2000; Gedek, 1999b]
3) Blocks transepithelial resistance and permeability changes, reverses impaired ZO-1 distribution and delays apoptosis of epithelial cells in response to EPEC	[Buts et al. 2006; Canil et al. 1993; Czerucka et al. 2000; Gedek, 1999b]
4) Dephosphorylates LPS from Escherichia coli strain O55B5	[Buts et al. 2006; Canil et al. 1993; Czerucka et al. 2000; Gedek, 1999b]

CT, cholera toxin; EHEC, enterohemorrhagic E. coli; EPEC, enteropathogenic E. coli; ERK, extracellular signal-regulated kinase; LPS, lipopolysaccharide; MAP, mitogen-activated protein; MLC, myosin light chain; NF-κB, nuclear factor kappa B; ZO-1, zonula occludens 1