title: Nonpathogenic Escherichia coli strain Nissle1917 prevents murine acute and chronic colitis.
abstract: BACKGROUND
  Nonpathogenic Escherichia coli strain Nissle1917 has been used as a probiotics in human inflammatory bowel disease; however, there are few reports examining its therapeutic effect on animal colitis models, and its therapeutic mechanisms remain unknown. The aim of this study was to elucidate the therapeutic effect and mechanism of Nissle1917 using murine acute and chronic colitis models.
  
  
  METHODS
  Two models were used. (1) Acute model: colitis was induced by administration of 1.3% dextran sodium sulfate for 7 days. Nissle1917 or phosphate-buffered saline were orally administered for 10 days. Mice were killed at day 10, and the colonic lesions were assessed macro- and microscopically. (2) Chronic model: IL-10 mice were treated with Nissle1917 or phosphate-buffered saline for 8 weeks. After 8 weeks of treatment, mice were killed to assess the colonic lesions macro- and microscopically. In the acute dextran sodium sulfate colitis model, viable, heat-killed, or genomic DNA of Nissle1917 was orally administered for 10 days, and the therapeutic effect was assessed.
  
  
  RESULTS
  In the acute model, Nissle1917 ameliorated body weight loss, disease activity index, and macro- and microscopic damage. In the chronic model, it also suppressed the mucosal inflammatory findings and histologic damages. Moreover, heat-killed Nissle1917 or its genomic DNA alone also ameliorated the acute DSS colitis and viable bacteria macro- and microscopically.
  
  
  CONCLUSIONS
  Nonpathogenic E. coli strain Nissle1917 prevents both acute and chronic colitis, and its anti-inflammatory effect is exhibited not only by viable bacteria but also by heat-killed bacteria or its DNA.
authors.affiliation: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Kamada
authors.forename: Nagamu
authors.initials: N
authors.lastname: Inoue
authors.forename: Tadakazu
authors.initials: T
authors.lastname: Hisamatsu
authors.forename: Susumu
authors.initials: S
authors.lastname: Okamoto
authors.forename: Katsuyoshi
authors.initials: K
authors.lastname: Matsuoka
authors.forename: Toshiro
authors.initials: T
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Chinen
authors.forename: Kyong Su
authors.initials: KS
authors.lastname: Hong
authors.forename: Takaya
authors.initials: T
authors.lastname: Yamada
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Suzuki
authors.forename: Noriaki
authors.initials: N
authors.lastname: Watanabe
authors.forename: Kanji
authors.initials: K
authors.lastname: Tsuchimoto
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Hibi
mesh_terms: D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D003092:Colitis / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004926:Escherichia coli; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D019936:Probiotics / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D000685:Serum Amyloid A Protein / Q000378:metabolism
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D000685:Serum Amyloid A Protein