<p>Beneficial effects of <em>Saccharomyces boulardii</em> CNCM I-745 on clinical disorders associated with intestinal barrier disruption</p>

Abstract

Intestinal barrier defects lead to “leaky gut syndrome”, defined as an increase in intestinal permeability that allows the passage of luminal content into intestinal tissue and the bloodstream. Such a compromised intestinal barrier is the main factor underlying the pathogenesis of inflammatory bowel disease, but also commonly occurs in various systemic diseases such as viral infections and metabolic syndrome. The non-pathogenic yeast Saccharomyces boulardii CNCM I-745 has demonstrated its effectiveness as a probiotic in the prevention and treatment of antibiotic-associated, infectious and functional diarrhea. Via multiple mechanisms of action implicated in intestinal barrier function, S. boulardii has beneficial effects on altered intestinal microbiota and epithelial barrier defects in different pathologies. The well-studied probiotic yeast S. boulardii plays a crucial role in the preservation and/or restoration of intestinal barrier function in multiple disorders. This could be of major interest in diseases characterized by alterations in intestinal barrier function.

Leaky gut: mechanisms, measurement and clinical implications in humans

“…There are several examples in the literature demonstrating diverse effects of bacteria and their products on intestinal barrier structure or function. Thus, Bifidobacteria enhance barrier function in experimental necrotising enterocolitis in mice,8 the yeast Saccharomyces boulardii has beneficial effects on altered intestinal microbiota and epithelial barrier defects in different pathologies,9 and different strains of Escherichia coli have opposite effects on the barrier: E. coli Nissle 1917 stimulates the tight junction protein ZO-2,10 11 whereas a prototypic translocating bacterium, E. coli strain C25, increases permeability 12. Products of the bacteria such as bacterial toxins, or bacterial dehydroxylation producing secondary bile acids and short-chain fatty acids produced by bacterial fermentation protect against bacteria or enhance the barrier function 13–15…”

Comparative immunophenotyping of Saccharomyces cerevisiae and Candida spp. strains from Crohn’s disease patients and their interactions with the gut microbiome

“…Furthermore, recent studies reported clear differences between adult and pediatric IBD patients’ gut fungal communities [ 8 ] and more heterogeneous fungal communities in CD patients compared to healthy subjects [ [23] , [24] , [25] , [26] ], suggesting a role of altered mycobiota in inflammatory diseases and “leaky gut” syndrome. Sokol and collaborators [ 23 ] observed a clear fungal dysbiosis in CD patients with an enrichment in Candida spp.…”

Saccharomyces Cerevisiae Var. Boulardii In Irritable Bowel Syndrome

“…Części drożdżaków udaje się przetrwać, a po dostaniu się do jelita wykazują trzy główne mechanizmy działania: działanie w świetle jelita, działanie troficzne oraz działanie przeciwzapalne na błonę śluzową [3,49] (Tabela I). [2,5,8,37,41,48,49,51,58,69,71,72]. Międzykomórkowe połączenia szczelinowe mogą być utrzymane dzięki ciągłej ekspresji E-kadheryny na powierzchni komórek.…”

“…Co więcej, zmniejsza stan zapalny poprzez uwięzienie limfocytów T pomocniczych produkujących interferon γ w węzłach chłonnych krezkowych. Dzięki temu ogranicza limfocytarny naciek zapalny i produkcję cytokin prozapalnych w jelitach [21,49,64,68,71]. Dochodzi też do stymulacji regulatorowych limfocytów T (ekspresja transformującego czynnika wzrostu beta TGF-β, który redukuje proces zapalny) i modyfikacji adherencji limfocytów do komórek endotelialnych, czyli usprawnienia toczenia się komórek i adhezji [41,66] Najnowsze techniki, szacujące ilość szczepów bakteryjnych w jelicie człowieka na 40 000, wykazują, że po antybiotykoterapii mikrobiota odnawia się w przeciągu 6-8 tygodni.…”