title: Natural colonization with Helicobacter species and the development of inflammatory bowel disease in interleukin-10-deficient mice.
abstract: BACKGROUND
  The interleukin-10-deficient (IL-10-/-) mice maintained in specific-pathogen-free (SPF) conditions develop typhlocolitis when experimentally infected with Helicobacter species. However, there is limited information regarding the role of Helicobacter species that naturally colonize IL-10-/- mice in typhlocolitis development. The aim of this study was to examine in SPF IL-10-/- mice the association between natural colonization specific Helicobacter species and typhlocolitis development.
  
  
  METHODS
  Cecum and proximal colon from 72 C57BL/6 x 129/Ola IL-10-/- mice (8-20 weeks old) were removed for DNA extraction and histologic evaluation. Genus-specific polymerase chain reaction- denaturing gradient gel electrophoresis (PCR-DGGE) and species-specific PCR were used to detect Helicobacter species. Mice were grouped by age, sex, and Helicobacter colonization status, and their histologic scores were compared. The development of clinical typhlocolitis was observed in a further 12 mice.
  
  
  RESULTS
  Species-specific PCR showed that mice were colonized with Helicobacter ganmani and/or Helicobacter hepaticus. The PCR-DGGE detected H. ganmani, H. hepaticus and an H. ganmani-like organism. The histologic scores in mice colonized with H. hepaticus were significantly higher than that in mice colonized with H. ganmani. Male mice showed significantly higher histologic scores than female mice. Four of the 12 mice developed clinical typhlocolitis in 38 weeks.
  
  
  CONCLUSIONS
  Natural colonization with different Helicobacter species was found in IL-10-/- mice within the same breeding colony. The severity of typhlocolitis differed according to the colonizing Helicobacter species. Furthermore, the rate of typhlocolitis development in IL-10-/- mice naturally colonized with Helicobacter species was significantly slower than that reported in experimentally infected mice.
authors.affiliation: The School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, Australia.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Danon
authors.forename: Martin
authors.initials: M
authors.lastname: Grehan
authors.forename: Vivian
authors.initials: V
authors.lastname: Chan
authors.forename: Adrian
authors.initials: A
authors.lastname: Lee
authors.forename: Hazel
authors.initials: H
authors.lastname: Mitchell
mesh_terms: D000818:Animals; D002432:Cecum / Q000382:microbiology / Q000473:pathology; D003106:Colon / Q000382:microbiology / Q000473:pathology; D004586:Electrophoresis / Q000379:methods; D005260:Female; D016998:Helicobacter / Q000145:classification* / Q000254:growth & development / Q000472:pathogenicity*; D015212:Inflammatory Bowel Diseases / Q000209:etiology* / Q000382:microbiology* / Q000473:pathology; D016753:Interleukin-10 / Q000172:deficiency* / Q000235:genetics / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016133:Polymerase Chain Reaction; D012720:Severity of Illness Index; D013045:Species Specificity
chemical_list: D016753:Interleukin-10