Florastor-Probiotic

 

Mechanisms of action of Saccharomyces boulardii

(The probiotic supplement known by trade name FLORASTOR).  Among the probiotics FLORASTOR is unique in it’s scope of actions documented by scientific research. Everyone should give serious consideration to adding it to their daily regimen.

Luminal action    Known effects of FLORASTOR within the GI tract itself
A) Antimicrobial activity
 1) Inhibition of growth of bacteria and parasites [Chen et al. 2006; Czerucka et al. 1994; Czerucka and Rampal, 2002; Dahan et al. 2003; Dalmasso et al. 2006a; Gedek, 1999a; Rigothier et al. 1994; Rodrigues et al. 1996; Mumy et al. 2008; Wu et al. 2008]
 2) Reduction of gut translocation of pathogens [Herek et al. 2004; Geyik et al. 2006]
 3) Neutralization of bacterial virulence factors [Buts et al. 1994; Jahn et al. 1996]
 4) Suppression of host cell adherence that interferes with bacterial colonization [Czerucka et al. 2000; Rodrigues et al. 1996; Wu et al. 2008]
B) Antitoxin effects
 1) Inhibition of toxin receptor binding sites [Buts et al. 2006; Castagliuolo et al. 1996, 1999; Czerucka et al. 2000; Tasteyre et al. 2002; Wu et al. 2008]
 2) Stimulation of antibody production against Clostridium difficile toxin A [Brandao et al. 1998; Qamar et al. 2001]
 3) Direct proteolysis of the pathogenic toxins/Secretion of enzymatic proteins [Buts et al. 2006; Castagliuolo et al. 1996; Pothoulakis et al. 1993]
  a) Produces a serine protease that cleaves C. difficile toxin A [Pothoulakis et al. 1993]
  b) Produces 63 kDa phosphatase that destroys the endotoxin of pathogenic Escherichia coli [Buts et al. 2006; Castagliuolo et al. 1996]
  c) Produces a 120 kDa protein that reduces the effects of cholera toxin [Czerucka et al. 1994]
C) Cross-talk with normal microbiota
When S. boulardii is given to antibiotic-exposed mice or patients with diarrhea, normal microbiota is re-established rapidly [Buts et al. 1986, 1999, 2006; Buts, 2009; Swidsinski et al. 2008]
Trophic action on the intestinal mucosa
 1) Reduces the number of infected cells and stimulates the growth and differentiation of intestinal cells in response to trophic factors [Barc et al. 2008; Swidsinski et al. 2008]
 2) Prevents apoptosis and synthesis of TNFα [Czerucka et al. 2000; Dahan et al. 2003; Dalmasso et al. 2006b]
 3) Reduces mucositis [Buts et al. 1986, 1999, 2006; Buts, 2009]
 4) Restores fluid transport pathways [Schneider et al. 2005]
 5) Stimulates protein and energy production and restores metabolic activities in colonic epithelial cells [Czerucka et al. 2007; Szajewska et al. 2007; Zanello et al. 2009]
 6) Secretes mitogenic factors that enhance cell restitution [Canonici et al. 2011]
 7) Enhances release of brush-border membrane enzymes [Buts et al. 1998, 2002; Schneider et al. 2005]
 8) Stimulates the production of glycoproteins in the brush border [Buts et al. 1990]
 9) Stimulates production of intestinal polyamines [Buts et al. 1986, 1994, 1999, 2002; Jahn et al. 1996; Schneider et al. 2005]
 10) Restores normal levels of colonic short chain fatty acids (SCFAs) [Buts et al. 1994; Sezer et al. 2009; Breves et al. 2000]
 11) Stabilizes gastrointestinal barrier function and strengthens enterocyte tight junctions [Czerucka et al. 2007; Dahan et al. 2003; Szajewska et al. 2007; Wu et al. 2008; Zanello et al. 2009]
 12) Reduces crypt hyperplasia and cell damage in colitis models [Wu et al. 2008]
 13) Decreases intestinal permeability in Crohn’s disease patients [Garcia et al. 2008]
Regulation of immune response
A) By acting as an immune stimulant
 S. boulardii effects on innate immunity
 1) Triggers activation of complement and migration of monocytes and granulocytes [Caetano et al. 1986]
 2) Enhances the number of Küpffer cells in germfree mice [Rodrigues et al. 2000]
 S. boulardii effects on adaptive immunity
 1) Enhances the mucosal immune response and secretory IgA intestinal levels [Buts et al. 1990; Czerucka et al. 2007; Generoso et al. 2011; Szajewska et al. 2007; Zanello et al. 2009]
 2) Enhances systemic immune response and levels of serum IgG to C. difficile toxins A and B. [Czerucka et al. 2007; Qamar et al. 2001]
 3) Contributes to earlier production of IFN-γ and IL-12 [Rodrigues et al. 2000; Thomas et al. 2009]
 4) Stimulates regulatory T cells [Jahn et al. 1996]
 5) Inhibits dendritic cell-induced activation of T cells [Dalmasso et al. 2006a]
 6) Modifies migration of lymphocytes in a chronic inflammatory bowel disease model [Dalmasso et al. 2006a]
 7) Modifies lymphocyte adherence to endothelial cells, improves cell rolling and adhesion [Dalmasso et al. 2006a]
B) By reducing pro-inflammatory responses and promoting mucosal anti-inflammatory signaling effects
 1) Decreases expression of pro-inflammatory cytokines (IL-8, IL-6, IL-1β, TNF-α and IFN-γ) [Dahan et al. 2003; Dalmasso et al. 2006a, 2006b; Mumy et al. 2008; Sougioultzis et al. 2006]
 2) Increases expression of the anti-inflammatory cytokine IL-10 [Generoso et al. 2011]
 3) Interferes with NF-κB-mediated signal transduction pathways, in immune and colonic epithelial cells [Buts, 2009; Dahan et al. 2003; Mumy et al. 2008; Pant et al. 2007; Sougioultzis et al. 2006]
 4) Blocks activation of ERK1/2 and MAP kinases [Chen et al. 2006; Kyne et al. 2001; Mumy et al. 2008; Sougioultzis et al. 2006]
 5) Decreases NO and inhibits production of inducible NOS [Girard et al. 2005]
 6) Modulates T cell migratory behavior and increases trapping of T helper cells into mesenteric lymph nodes [Dalmasso et al. 2006a; Fidan et al. 2009; Sougioultzis et al. 2006; Thomas et al. 2009]
 7) Stimulates production of anti-inflammatory molecules in human colonocytes such as PPAR-γ [Chen et al. 2006; Lee et al. 2005, 2009; Mumy et al. 2008]
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