Mechanisms of action
An advantage of probiotics is that they are living organisms incorporating a delivery system (most probiotics survive to the target organ) bringing an arsenal of anti-pathogenic strategies into play. S. boulardii has several different types of mechanisms of action (Figure (Figure2)2) which may be classified into three main areas: luminal action, trophic action and mucosal-anti-inflammatory signaling effects[8,75-77]. Within the intestinal lumen, S. boulardii may interfere with pathogenic toxins, preserve cellular physiology, interfere with pathogen attachment, interact with normal microbiota or assist in reestablishing short chain fatty acid levels. S. boulardii also may act as an immune regulator, both within the lumen and systemically.
Anti-toxin effects: S. boulardii may interfere with pathogenesis within the intestinal lumen by several mechanisms: either by blocking pathogen toxin receptor sites[78], or acting as a decoy receptor for the pathogenic toxin[79] or by direct destruction of the pathogenic toxin. Castagliuolo et al[80] found a 54 kDa serine protease produced by S. boulardii directly degrades C. difficile toxin A and B. The efficacy of other strains of Saccharomyces has also been investigated. Only S. boulardii produces a protease capable of degrading Clostridium difficile toxins and receptors sites on the enterocyte cell surface, unlike other strains of Saccharomyces[78,81]. Buts et al[82] found a 63 kDa phosphatase produced by S. boulardii destroys the endotoxin of pathogenic E. coli. Several investigators showed that S. boulardii could reduce the effects of cholera toxin and this may be due to a 120 kDa protein produced by S. boulardii[83,84].
Antimicrobial activity: S. boulardii is capable of directly or indirectly interfering with intestinal pathogens. S. boulardii may directly inhibit the growth of pathogens (such as Candida albicans, Salmonella typhimurum, Yersinia enterocolitium, Aeromonas hemolysin[43,85,86]). In animal models testing for the ability to inhibit pathogen growth, several studies using non-S. boulardii strains of S. cerevisiae did not find any effect unlike the protective effects of S. boulardii[31,70]. [...] S. boulardii may also act by enhancing the integrity of the tight junction between enterocytes, thus preserving intestinal integrity and function[87,88]. Wu et al[88] found less crypt hyperplasia and cell damage in a Citrobacter rodentium-induced mice model of colitis when mice were treated with 1 × 109 S. boulardii per day for 7 d. Garcia Vilela et al[62] found decreased intestinal permeability when patients with Crohn’s disease were given S. boulardii (1.6 × 109/d for 4 mo) compared with placebo. S. boulardii has also been shown to reduce the translocation of pathogens in rat and pig animal models[64,89,90]. S. boulardii can also interfere with pathogenic attachment to intestinal receptor sites[88,91,92]. Gedek et al[93] also found that S. boulardii acts as a decoy by causing EPEC cells to directly bind to the surface of S. boulardii cells rather than enterocytes.
Cross-talk with normal microbiota: Newer techniques, including metagenomics and PCR probes have documented that a typical human may carry over 40 000 bacterial species in the collective intestinal microbiome[94]. The normal intestinal flora has many functions, including digestion of food, but the one that is most germane for this discussion is called “colonization resistance”[77,95,96]. This involves the interaction of many bacterial microflora and results in a barrier effect against colonization of pathogenic organisms. Normal microflora may act by competitive exclusion of nutrients or attachment sites, produce bacteriocins, or produce enzymes detrimental to pathogenic growth. Factors that disrupt this protective barrier, for example antibiotic use or surgery, results in host susceptibility to pathogen colonization until such time as the normal microflora can become re-established. Typically, it takes six to eight weeks for normal microbiota to recover after antibiotic exposure or disease resolution[97]. Probiotics are uniquely qualified to fit into this window of susceptibility and may act as surrogate normal microflora until recovery is achieved. S. boulardii has no effect on normal microbiota in healthy human controls[98,99]. In contrast, when S. boulardii is given to antibiotic-shocked mice or patients with diarrhea, normal microbiota is re-established rapidly[99,100].
Restoration of metabolic activities: S. boulardii has been shown to be able to increase short chain fatty acids (SCFA), which are depressed during disease, indicating altered colonic fermentation[98,101,102].
Trophic effects: S. boulardii can reduce mucositis[103], restore fluid transport pathways[84,101,104], stimulate protein and energy production[105], or act through a trophic effect by releasing spermine and spermidine or other brush border enzymes that aid in the maturation of enterocytes[106,107].
Immune response: S. boulardii may also regulate immune responses, either acting as an immune stimulant or by reducing pro-inflammatory responses. S. boulardii may cause an increase in secretory IgA levels in the intestine[56,108-110]. It has also been found associated with higher levels of serum IgG to C. difficile toxins A and B[111]. S. boulardii may also interfere with NF-κB-mediated signal transduction pathways, which stimulate pro-inflammatory cytokine production[76,112,113]. Chen et al[114] found that S. boulardii blocks activation of ERK1/2 and MAP kinases, which typically stimulate IL-8 production and cell necrosis in mice ileal loop models and in in vitro models. S. boulardii has also been shown to cause the trapping of T helper cells into mesenteric lymph nodes, thereby reducing inflammation[115].
Unfortunately, I live in a landlocked country, so the sea is quite far away. 
