title: Saccharomyces boulardii improves intestinal epithelial cell restitution by inhibiting αvβ5 integrin activation state.
abstract: Intestinal epithelial cell damage is frequently seen in the mucosal lesions of infectious or inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. Complete remission of these diseases requires both the disappearance of inflammation and the repair of damaged epithelium. Saccharomyces boulardii (Sb, Biocodex) is a non-pathogenic yeast widely used as a preventive and therapeutic probiotic for the prevention and treatment of diarrhea and other gastrointestinal disorders. We recently showed that it enhances the repair of intestinal epithelium through activation of α2β1 integrin collagen receptors. In the present study, we demonstrated that α2β1 integrin is not the sole cell-extracellular matrix receptor involved during Sb-mediated intestinal restitution. Indeed, by using cell adhesion assays, we showed that Sb supernatant contains heat sensitive molecule(s), with a molecular weight higher than 9 kDa, which decreased αvβ5 integrin-mediated adhesion to vitronectin by competing with the integrin. Moreover, Sb-mediated changes in cell adhesion to vitronectin resulted in a reduction of the αvβ5signaling pathway. We used a monolayer wounding assay that mimics in vivo cell restitution to demonstrate that down-modulation of the αvβ5 integrin-vitronectin interaction is related to Sb-induced cell migration. We therefore postulated that Sb supernatant contains motogenic factors that enhance cell restitution through multiple pathways, including the dynamic fine regulation of αvβ5 integrin binding activity. This could be of major importance in diseases characterized by severe mucosal injury, such as inflammatory and infectious bowel diseases.
authors.affiliation: Aix-Marseille Université, Centre de Recherche en Oncologie et Oncopharmacologie, Marseille, France ; Inserm UMR 9111, Marseille, France.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Canonici
authors.forename: Emilie
authors.initials: E
authors.lastname: Pellegrino
authors.forename: Carole
authors.initials: C
authors.lastname: Siret
authors.forename: Chloé
authors.initials: C
authors.lastname: Terciolo
authors.forename: Dorota
authors.initials: D
authors.lastname: Czerucka
authors.forename: Sonia
authors.initials: S
authors.lastname: Bastonero
authors.forename: Jacques
authors.initials: J
authors.lastname: Marvaldi
authors.forename: Dominique
authors.initials: D
authors.lastname: Lombardo
authors.forename: Véronique
authors.initials: V
authors.lastname: Rigot
authors.forename: Frédéric
authors.initials: F
authors.lastname: André
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D045744:Cell Line, Tumor; D002465:Cell Movement; D020895:Enterocytes / Q000166:cytology / Q000378:metabolism* / Q000382:microbiology*; D005247:Feeding Behavior; D005260:Female; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D008970:Molecular Weight; D011485:Protein Binding; D021381:Protein Transport; D019030:Receptors, Vitronectin / Q000378:metabolism*; D012440:Saccharomyces / Q000502:physiology*; D015398:Signal Transduction; D019096:Vitronectin / Q000378:metabolism
chemical_list: D019030:Receptors, Vitronectin; D019096:Vitronectin; C064660:integrin alphaVbeta5