title: Effectiveness of Saccharomyces boulardii in a rat model of colitis.
abstract: OBJECTIVE
  To investigate the effects of Saccharomyces boulardii (S. boulardii) in an experimental rat model of trinitrobenzene sulfonic acid (TNBS)-induced colitis.
  
  
  METHODS
  Thirty-two Wistar albino female rats were categorized into five groups. On the first day of the study, 50 mg TNBS was administered via a rectal catheter in order to induce colitis in all rats, except those in the control group. For 14 d, the rats were fed a standard diet, without the administration of any additional supplements to either the control or TNBS groups, in addition to 1 mg/kg per day S. boulardii to the S. boulardii group, 1 mg/kg per day methyl prednisolone (MP) to the MP group. The animals in the S. boulardii + MP group were coadministered these doses of S. boulardii and MP. During the study, weight loss, stool consistency, and the presence of obvious blood in the stool were evaluated, and the disease activity index (DAI) for colitis was recorded. The intestines were examined and colitis was macro- and microscopically scored. The serum and tissue levels of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) were determined, and fungemia was evaluated in the blood samples.
  
  
  RESULTS
  The mean DAI scores for the MP and S. boulardii + MP groups was significantly lower than the TNBS group (3.69 ± 0.61 vs 4.46 ± 0.34, P = 0.018 and 3.77 ± 0.73 vs 4.46 ± 0.34, P = 0.025, respectively). While no significant differences between the TNBS and the S. boulardii or MP groups could be determined in terms of serum NO levels, the level of serum NO in the S. boulardii + MP group was significantly higher than in the TNBS and S. boulardii groups (8.12 ± 4.25 μmol/L vs 3.18 ± 1.19 μmol/L, P = 0.013; 8.12 ± 4.25 μmol/L vs 3.47 ± 1.66 μmol/L, P = 0.012, respectively). The tissue NO levels in the S. boulardii, MP and S. boulardii + MP groups were significantly lower than the TNBS group (16.62 ± 2.27 μmol/L vs 29.72 ± 6.10 μmol/L, P = 0.002; 14.66 ± 5.18 μmol/L vs 29.72 ± 6.10 μmol/L, P = 0.003; 11.95 ± 2.34 μmol/L vs 29.72 ± 6.10 μmol/L, P = 0.002, respectively). The tissue NO levels in the S. boulardii, MP and S. boulardii + MP groups were similar. The mean serum and tissue TNF-α levels were determined to be 12.97 ± 18.90 pg/mL and 21.75 ± 15.04 pg/mL in the control group, 18.25 ± 15.44 pg/mL and 25.27 ± 11.95 pg/mL in the TNBS group, 20.59 ± 16.15 pg/mL and 24.39 ± 13.06 pg/mL in the S. boulardii group, 9.05 ± 5.13 pg/mL and 24.46 ± 10.85 pg/mL in the MP group, and 13.95 ± 10.17 pg/mL and 24.26 ± 10.37 pg/mL in the S. boulardii + MP group. Significant differences in terms of the levels of serum and tissue TNF-α and the macroscopic and microscopic scores were not found between the groups. S. boulardii fungemia was not observed in any of the rats. However, Candida fungemia was detected in one rat (14%) in the TNBS group, two rats (28%) in the S. boulardii group, three rats (50%) in the MP group, and three rats (42%) in S. boulardii + MP group.
  
  
  CONCLUSIONS
  S. boulardii does not demonstrate considerable effects on the DAI, pathological scores, or cytokine levels but does decrease the tissue NO levels.
authors.affiliation: Department of Gastroenterology, Dokuz Eylul University School of Medicine, Inciralti, Izmir 35340, Turkey. mujde.soyturk@deu.edu.tr
authors.forename: Mujde
authors.initials: M
authors.lastname: Soyturk
authors.forename: Saba Mukaddes
authors.initials: SM
authors.lastname: Saygili
authors.forename: Huseyin
authors.initials: H
authors.lastname: Baskin
authors.forename: Ozgul
authors.initials: O
authors.lastname: Sagol
authors.forename: Osman
authors.initials: O
authors.lastname: Yilmaz
authors.forename: Fatih
authors.initials: F
authors.lastname: Saygili
authors.forename: Hale
authors.initials: H
authors.lastname: Akpinar
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D003092:Colitis / Q000097:blood / Q000139:chemically induced / Q000382:microbiology / Q000473:pathology / Q000628:therapy*; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D005765:Gastrointestinal Agents / Q000494:pharmacology; D018836:Inflammation Mediators / Q000097:blood; D008775:Methylprednisolone / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood; D019936:Probiotics; D051381:Rats; D017208:Rats, Wistar; D012440:Saccharomyces / Q000254:growth & development*; D013997:Time Factors; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D005765:Gastrointestinal Agents; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D014302:Trinitrobenzenesulfonic Acid; D008775:Methylprednisolone