title: Saccharomyces cerevisiae modulates immune gene expressions and inhibits ETEC-mediated ERK1/2 and p38 signaling pathways in intestinal epithelial cells.
abstract: BACKGROUND
  Enterotoxigenic Escherichia coli (ETEC) infections result in large economic losses in the swine industry worldwide. ETEC infections cause pro-inflammatory responses in intestinal epithelial cells and subsequent diarrhea in pigs, leading to reduced growth rate and mortality. Administration of probiotics as feed additives displayed health benefits against intestinal infections. Saccharomyces cerevisiae (Sc) is non-commensal and non-pathogenic yeast used as probiotic in gastrointestinal diseases. However, the immuno-modulatory effects of Sc in differentiated porcine intestinal epithelial cells exposed to ETEC were not investigated.
  
  
  RESULTS
  We reported that the yeast Sc (strain CNCM I-3856) modulates transcript and protein expressions involved in inflammation, recruitment and activation of immune cells in differentiated porcine intestinal epithelial IPEC-1 cells. We demonstrated that viable Sc inhibits the ETEC-induced expression of pro-inflammatory transcripts (IL-6, IL-8, CCL20, CXCL2, CXCL10) and proteins (IL-6, IL-8). This inhibition was associated to a decrease of ERK1/2 and p38 MAPK phosphorylation, an agglutination of ETEC by Sc and an increase of the anti-inflammatory PPAR-γ nuclear receptor mRNA level. In addition, Sc up-regulates the mRNA levels of both IL-12p35 and CCL25. However, measurement of transepithelial electrical resistance displayed that Sc failed to maintain the barrier integrity in monolayer exposed to ETEC suggesting that Sc does not inhibit ETEC enterotoxin activity.
  
  
  CONCLUSIONS
  Sc (strain CNCM I-3856) displays multiple immuno-modulatory effects at the molecular level in IPEC-1 cells suggesting that Sc may influence intestinal inflammatory reaction.
authors.affiliation: Société Industrielle Lesaffre, Lesaffre Feed Additives, Marcq-en-Baroeul, France.
authors.forename: Galliano
authors.initials: G
authors.lastname: Zanello
authors.forename: Mustapha
authors.initials: M
authors.lastname: Berri
authors.forename: Joëlle
authors.initials: J
authors.lastname: Dupont
authors.forename: Pierre-Yves
authors.initials: PY
authors.lastname: Sizaret
authors.forename: Romain
authors.initials: R
authors.lastname: D'Inca
authors.forename: Henri
authors.initials: H
authors.lastname: Salmon
authors.forename: François
authors.initials: F
authors.lastname: Meurens
mesh_terms: D000371:Agglutination; D000818:Animals; D002454:Cell Differentiation; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism / Q000382:microbiology; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D018920:Coculture Techniques; D054307:Enterotoxigenic Escherichia coli / Q000502:physiology*; D005786:Gene Expression Regulation / Q000276:immunology*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D007413:Intestinal Mucosa / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D020935:MAP Kinase Signaling System / Q000276:immunology*; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D010766:Phosphorylation; D019936:Probiotics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000276:immunology*; D013552:Swine; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D018925:Chemokines; D015850:Interleukin-6; D016209:Interleukin-8; D012333:RNA, Messenger; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases