title: Saccharomyces boulardii inhibits inflammatory bowel disease by trapping T cells in mesenteric lymph nodes.
abstract: OBJECTIVE
  Saccharomyces boulardii is a nonpathogenic yeast used for treatment of diarrhea. We used a mice model of inflammatory bowel disease (IBD) to analyze the effects of S boulardii on inflammation.
  
  
  METHODS
  Lymphocyte-transferred SCID mice, displaying IBD, were fed daily with S boulardii. Weight loss and inflammatory status of the colon were monitored. Nuclear factor-kappaB activity was assessed in the colon. The CD4(+) T-cell production of interferon (IFN) gamma was evaluated by enzyme-linked immunosorbent assay, and a comprehensive reverse-transcription polymerase chain reaction (RT-PCR) analysis for both colon and mesenteric lymph nodes was performed. Finally, we analyzed cell migration mechanisms in vitro and in vivo.
  
  
  RESULTS
  S boulardii treatment inhibits IBD. S boulardii induces an accumulation of IFN-gamma-producing T-helper 1 cells within the mesenteric lymph nodes correlated with a diminution of CD4(+) T-cell number and IFN-gamma production by CD4+ T cells within the colon. The influence of S boulardii treatment on cell accumulation in mesenteric lymph nodes was also observed in normal BALB/c mice and involves modifications of lymph node endothelial cell adhesiveness by a yeast secretion product.
  
  
  CONCLUSIONS
  S boulardii has a unique action on inflammation by a specific alteration of the migratory behavior of T cells, which accumulate in mesenteric lymph nodes. Therefore, S boulardii treatment limits the infiltration of T-helper 1 cells in the inflammed colon and the amplification of inflammation induced by proinflammatory cytokines production. These results suggest that S boulardii administration may have a beneficial effect in the treatment of IBD.
authors.affiliation: Laboratoire de Gastroentérologie, Faculté de Médecine, IFR50, UNSA, Nice, France.
authors.forename: Guillaume
authors.initials: G
authors.lastname: Dalmasso
authors.forename: Françoise
authors.initials: F
authors.lastname: Cottrez
authors.forename: Véronique
authors.initials: V
authors.lastname: Imbert
authors.forename: Patricia
authors.initials: P
authors.lastname: Lagadec
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Peyron
authors.forename: Patrick
authors.initials: P
authors.lastname: Rampal
authors.forename: Dorota
authors.initials: D
authors.lastname: Czerucka
authors.forename: Hervé
authors.initials: H
authors.lastname: Groux
authors.forename: Arnaud
authors.initials: A
authors.lastname: Foussat
authors.forename: Valerie
authors.initials: V
authors.lastname: Brun
mesh_terms: D000818:Animals; D001835:Body Weight / Q000502:physiology; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology*; D002465:Cell Movement / Q000502:physiology; D004195:Disease Models, Animal; D007249:Inflammation / Q000382:microbiology*; D015212:Inflammatory Bowel Diseases / Q000473:pathology / Q000517:prevention & control*; D007371:Interferon-gamma / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D008198:Lymph Nodes / Q000166:cytology / Q000382:microbiology / Q000473:pathology*; D008643:Mesentery / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D016328:NF-kappa B / Q000378:metabolism; D019936:Probiotics / Q000627:therapeutic use; D012440:Saccharomyces / Q000502:physiology*; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology
chemical_list: D016328:NF-kappa B; D007371:Interferon-gamma