title: Variable response to probiotics in two models of experimental colitis in rats.
abstract: OBJECTIVE
  Clinical and experimental data suggest an important role for intestinal microflora in the pathogenesis of inflammatory bowel disease, and probiotics have been shown to ameliorate pouchitis. We evaluated the effect of different preparations of probiotic bacteria on experimental colitis in rats.
  
  
  METHODS
  Rats were treated daily intragastrically with two probiotic preparations, VSL#3 or strain GG (LGG), 7 days before induction of colitis and for another week thereafter. Colitis was induced by intracolonic administration of either dinitrobenzene sulfonic acid (DNBS) or iodoacetamide. Rats were killed 7 days after induction of colitis, the colon isolated, washed, weighed, lesion area measured, and mucosa processed for determination of myeloperoxidase (MPO) and nitric oxide synthase (NOS) activities and prostaglandin E2 (PGE2) generation.
  
  
  RESULTS
  In rats cotreated with VSL#3 or LGG and iodoacetamide, there was a significant decrease in the lesion area, 98 +/- 37 mm and 142 +/- 43 mm, respectively, as compared with 342 +/- 66 mm in the control group. Colonic wet weight significantly decreased to 1.3 +/- 0.1 g/10 cm and 1.4 +/- 0.1 g/10 cm, respectively, as compared with 1.7 +/- 0.1 g/10 cm. There was also a significant decrease in PGE2 generation, MPO, and NOS activities in the VSL#3 and LGG treatment groups. Presence of VSL#3 bacteria in the rat's colon was confirmed by culture and polymerase chain reaction (PCR) amplification. Neither probiotic preparation had an effect on the extent of colonic damage in DNBS-induced colitis.
  
  
  CONCLUSIONS
  Both VSL#3 and LGG significantly ameliorated colitis induced by the sulfhydryl-blocker iodoacetamide, but had no effect on the immune-mediated DNBS-induced colitis. The results suggest a possible role for sulfhydryl compounds in the protective effect of probiotic bacteria, and support their use in patients with inflammatory bowel disease.
authors.affiliation: Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem. shibolet@hadassah.org.il
authors.forename: Oren
authors.initials: O
authors.lastname: Shibolet
authors.forename: Fanny
authors.initials: F
authors.lastname: Karmeli
authors.forename: Rami
authors.initials: R
authors.lastname: Eliakim
authors.forename: Erwin
authors.initials: E
authors.lastname: Swennen
authors.forename: Patrizia
authors.initials: P
authors.lastname: Brigidi
authors.forename: Paulo
authors.initials: P
authors.lastname: Gionchetti
authors.forename: Massimo
authors.initials: M
authors.lastname: Campieri
authors.forename: Sara
authors.initials: S
authors.lastname: Morgenstern
authors.forename: Daniel
authors.initials: D
authors.lastname: Rachmilewitz
mesh_terms: D000477:Alkylating Agents / Q000009:adverse effects*; D000818:Animals; D001557:Benzenesulfonates / Q000009:adverse effects*; D001644:Bifidobacterium; D003092:Colitis / Q000139:chemically induced* / Q000188:drug therapy* / Q000276:immunology; D004195:Disease Models, Animal; D007413:Intestinal Mucosa / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D007460:Iodoacetamide / Q000009:adverse effects*; D007778:Lactobacillus; D008297:Male; D019936:Probiotics / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013291:Streptococcus
chemical_list: D000477:Alkylating Agents; D001557:Benzenesulfonates; C007488:dinitrobenzenesulfonic acid; D007460:Iodoacetamide