title: Bacteria and spontaneous experimental colitis: immunological changes.
abstract: BACKGROUND
  Intestinal commensal flora seems to be a requisite for both human and experimental intestinal inflammation. Our aim was to assess the immunological changes in the colon of IL-10(-/-) mice depending on the environmental conditions.
  
  
  METHODS
  Twelve wild-type (WT) and 24 IL-10(-/-) 4-week-old mice were kept under specific pathogen-free (SPF) conditions for 4 weeks. Half of them were transferred to a conventional environment. Mice were sacrificed at 12 weeks of age, and the incidence and severity of colitis was assessed. Intraepithelial (IEL) and lamina propria (LPL) lymphocytes were assessed for phenotype and apoptosis by flow cytometry. Toll-like receptors 2 (TLR2) and TLR9 expression was assessed by real-time PCR. Immunohistochemical analyses for cell apoptosis, TLR2 and MyD88 were also performed.
  
  
  RESULTS
  IL-10(-/-) mice shifted to conventional conditions showed a greater incidence (66% vs. 50%) and severity of colitis than animals kept under SPF conditions (P = 0·009). The number of CD3+ IEL was higher and their apoptosis rate lower in IL-10(-/-) than in their WT counterparts, regardless of the environment. In LPL, however, these differences were only observed in mice shifted to conventional conditions. TLR2 expression was significantly increased in SPF-housed IL-10(-/-) mice when compared to WT controls. Immunohistochemistry demonstrated the loss of TLR2 and MyD88 in damaged areas.
  
  
  CONCLUSIONS
  In SPF conditions, IL-10 deficiency appears to be compensated by an increased epithelial TLR2 expression, thus resulting in a milder colonic damage. However, in conventional conditions, this compensatory mechanism would be exceeded inducing a more severe colonic damage with activation of LPL immune cells.
authors: Health Sciences Research Institute, Germans Trias i Pujol, Badalona, Spain.
authors: Elisabet
authors: E
authors: Pedrosa
authors: Violeta
authors: V
authors: Lorén
authors: Eduard
authors: E
authors: Cabré
authors: Eugeni
authors: E
authors: Doménech
authors: Isabel
authors: I
authors: Ojanguren
authors: Miquel A
authors: MA
authors: Gassull
authors: Josep
authors: J
authors: Mañé
mesh_terms: D000818:Animals; D017209:Apoptosis; D001419:Bacteria / Q000235:genetics / Q000276:immunology*; D003092:Colitis / Q000276:immunology* / Q000382:microbiology; D004195:Disease Models, Animal; D005434:Flow Cytometry; D006801:Humans; D016753:Interleukin-10 / Q000172:deficiency*; D007413:Intestinal Mucosa / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D018709:Statistics, Nonparametric; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D051217:Toll-Like Receptor 9 / Q000235:genetics
chemical_list: C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; C495370:Tlr9 protein, mouse; D051195:Toll-Like Receptor 2; D051217:Toll-Like Receptor 9; D016753:Interleukin-10