Saccharomyces boulardii inhibits inflammatory bowel disease by trapping T cells in mesenteric lymph nodes

被引:127
作者
Dalmasso, Guillaume
Cottrez, Francoise
Imbert, Veronique
Lagadec, Patricia
Peyron, Jean-Francois
Rampal, Patrick
Czerucka, Dorota
Groux, Herve
机构
[1] UNSA, Fac Med, Lab Gastroenterol, IFR50, Nice, France
[2] UNSA, Hop Archet, INSERM, U576, Nice, France
[3] UNSA, Fac Med, IFR50, INSERM,U526, Nice, France
[4] Hop Princesse Grace, Serv Gastroenterol, Monaco, Monaco
关键词
D O I
10.1053/j.gastro.2006.10.001
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: 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-kappa B 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 I 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 I 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.
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页码:1812 / 1825
页数:14
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共 56 条
  • [1] Yogurt and gut function
    Adolfsson, O
    Meydani, SN
    Russell, RM
    [J]. AMERICAN JOURNAL OF CLINICAL NUTRITION, 2004, 80 (02) : 245 - 256
  • [2] Management of ulcerative colitis and Crohn's disease
    Baert, F
    Vermeire, S
    Noman, M
    Van Assche, G
    Haens, GD
    Rutgeerts, P
    [J]. ACTA CLINICA BELGICA, 2004, 59 (05) : 304 - 314
  • [3] Chemokines and leukocyte traffic
    Baggiolini, M
    [J]. NATURE, 1998, 392 (6676) : 565 - 568
  • [4] Robiotics, prebiotics or 'conbiotics'?
    Berg, RD
    [J]. TRENDS IN MICROBIOLOGY, 1998, 6 (03) : 89 - 92
  • [5] Calcium influx and signaling in yeast stimulated by intracellular sphingosine 1-phosphate accumulation
    Birchwood, CJ
    Saba, JD
    Dickson, RC
    Cunningham, KW
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (15) : 11712 - 11718
  • [6] DISPOSITION KINETICS OF SACCHAROMYCES-BOULARDII IN MAN AND RAT
    BLEHAUT, H
    MASSOT, J
    ELMER, GW
    LEVY, RH
    [J]. BIOPHARMACEUTICS & DRUG DISPOSITION, 1989, 10 (04) : 353 - 364
  • [7] The immunological and genetic basis of inflammatory bowel disease
    Bouma, G
    Strober, W
    [J]. NATURE REVIEWS IMMUNOLOGY, 2003, 3 (07) : 521 - 533
  • [8] CARTERMJ, 2004, GUT, V53, pV1
  • [9] Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa
    Castagliuolo, I
    Riegler, MF
    Valenick, L
    LaMont, JT
    Pothoulakis, C
    [J]. INFECTION AND IMMUNITY, 1999, 67 (01) : 302 - 307
  • [10] PAR2 activation alters colonic paracellular permeability in mice via IFN-γ-dependent and -independent pathways
    Cenac, N
    Chin, AC
    Garcia-Villar, R
    Salvador-Cartier, C
    Ferrier, L
    Vergnolle, N
    Buret, AG
    Fioramonti, J
    Bueno, L
    [J]. JOURNAL OF PHYSIOLOGY-LONDON, 2004, 558 (03): : 913 - 925