title: Bacteroides vulgatus protects against Escherichia coli-induced colitis in gnotobiotic interleukin-2-deficient mice.
abstract: OBJECTIVE
  The microflora plays a crucial role in inflammatory bowel diseases (IBDs). Specific pathogen-free (SPF), but not germ-free, interleukin (IL)-2-deficient (IL-2-/-) mice develop colitis. The colitogenicity of commensal bacteria was determined.
  
  
  METHODS
  Gnotobiotic IL-2-/- and IL-2+/+ mice were colonized with Escherichia coli mpk, Bacteroides vulgatus mpk, or both bacterial strains, or with E. coli strain Nissle 1917. DNA arrays were used to characterize E. coli mpk. Colitis was analyzed by histology and real-time reverse-transcription polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, IL-10, and CD14 messenger RNA (mRNA) expression. Bacterial numbers in feces and bacterial localization in the colon was determined by culture and fluorescence in situ hybridization (FISH).
  
  
  RESULTS
  IL-2-/- but not IL-2+/+ mice monocolonized with E. coli mpk developed colitis, whereas mono-association with B. vulgatus mpk, or E. coli Nissle, or co-colonization with E. coli mpk and B. vulgatus mpk, did not induce colitis. DNA array experiments and cellular studies revealed that E. coli mpk is a nonpathogenic strain. FISH and culture methods revealed that the anticolitogenic effect of B. vulgatus mpk on E. coli mpk cannot be explained by a significant reduction in numbers of E. coli in the colon. E. coli mpk-induced colitis was associated with increased IFN-gamma, TNF-alpha, CD14, and IL-10 mRNA expression in the colon.
  
  
  CONCLUSIONS
  In IL-2-/- mice, B. vulgatus mpk protects against E. coli mpk-triggered colitis by an unknown mechanism. E. coli Nissle does not induce colitis. Various bacterial species common to the microflora differ in their ability to trigger IBD.
authors.affiliation: Institut für Medizinische Mikrobiologie und Krankenhaushygiene, Eberhard Karls-Universität, Tübingen, Germany.
authors.forename: Marc
authors.initials: M
authors.lastname: Waidmann
authors.forename: Oliver
authors.initials: O
authors.lastname: Bechtold
authors.forename: Julia-Stefanie
authors.initials: JS
authors.lastname: Frick
authors.forename: Hans-Anton
authors.initials: HA
authors.lastname: Lehr
authors.forename: Sören
authors.initials: S
authors.lastname: Schubert
authors.forename: Ulrich
authors.initials: U
authors.lastname: Dobrindt
authors.forename: Jürgen
authors.initials: J
authors.lastname: Loeffler
authors.forename: Erwin
authors.initials: E
authors.lastname: Bohn
authors.forename: Ingo B
authors.initials: IB
authors.lastname: Autenrieth
mesh_terms: D000818:Animals; D001439:Bacteroides / Q000254:growth & development*; D003092:Colitis / Q000382:microbiology* / Q000503:physiopathology / Q000517:prevention & control; D004926:Escherichia coli / Q000254:growth & development*; D004927:Escherichia coli Infections / Q000382:microbiology* / Q000503:physiopathology / Q000517:prevention & control; D005243:Feces / Q000382:microbiology; D005260:Female; D015870:Gene Expression; D005856:Germ-Free Life; D007376:Interleukin-2 / Q000235:genetics*; D007422:Intestines / Q000382:microbiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D013047:Specific Pathogen-Free Organisms
chemical_list: D007376:Interleukin-2