Table 2.
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