title: Soluble beta-1,3/1,6-glucan from yeast inhibits experimental periodontal disease in Wistar rats.
abstract: OBJECTIVE
  We have investigated whether a purified immunomodulatory water soluble beta-1,3/1,6-glucan isolated from the cell wall of Bakers yeast, Saccharomyces cerevisiae, would influence the progression of ligature-induced periodontal disease, and to modulate accompanying cytokine and hypothalamic-pituitary-adrenal (HPA) axis responses to a lipopolysaccharide (LPS) challenge.
  
  
  METHODS
  beta-1,3/1,6-glucan (10 mg/kg/day) was given in the drinking water to Wistar rats during the entire experiment, starting 14 days before disease induction, while control rats were given tap water only. Periodontal disease was assessed when the ligatures had been in place for 35 days.
  
  
  RESULTS
  Orally administered soluble beta-1,3/1,6-glucan significantly reduced periodontal bone loss as measured on digital X-rays (p=0,026). Glucan-treated rats also showed a significantly enhanced plasma level of the HPA axis-driven hormone corticosterone (p=0.047), and of the cytokine transforming growth factor-1beta (p=0.032), as well as a tendency to enhanced IL-10 (p=0.106), induced by intra-peritoneally administered LPS.
  
  
  CONCLUSIONS
  Soluble beta-1,3/1,6-glucan administered by the oral route diminishes ligature-induced periodontal bone loss in this model. This effect may be attributable to the well documented ability of beta-1,3/1,6-glucan to stimulate macrophage phagocytosis and to skew the T helper (Th)1/Th2 balance towards Th1 and T regulatory responses. The HPA axis may play a significant role in beta-1,3/1,6-glucan induced immune modulation.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, University of Oslo, Oslo, Norway. tbreivik@odont.uio.no
authors.forename: Torbjørn
authors.initials: T
authors.lastname: Breivik
authors.forename: Per Kristian
authors.initials: PK
authors.lastname: Opstad
authors.forename: Rolf
authors.initials: R
authors.lastname: Engstad
authors.forename: Glenn
authors.initials: G
authors.lastname: Gundersen
authors.forename: Per
authors.initials: P
authors.lastname: Gjermo
authors.forename: Hans
authors.initials: H
authors.lastname: Preus
mesh_terms: D016301:Alveolar Bone Loss / Q000188:drug therapy / Q000276:immunology; D000818:Animals; D003345:Corticosterone / Q000097:blood; D005936:Glucans / Q000627:therapeutic use*; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D016753:Interleukin-10 / Q000097:blood; D008026:Ligation; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D010510:Periodontal Diseases / Q000188:drug therapy* / Q000276:immunology; D010913:Pituitary-Adrenal System / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012441:Saccharomyces cerevisiae; D016212:Transforming Growth Factor beta / Q000097:blood; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D047071:beta-Glucans / Q000627:therapeutic use*
chemical_list: D005936:Glucans; D008070:Lipopolysaccharides; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D047071:beta-Glucans; C033671:epiglucan; D016753:Interleukin-10; D003345:Corticosterone