title: Oral microbiome composition changes in mouse models of colitis.
abstract: OBJECTIVE
  Oral mucosal pathologies are frequent in inflammatory bowel disease (IBD). Since host-microbiome interactions are implicated in the pathogenesis of IBD, in this study the potential for changes affecting the oral microbiome was evaluated using two complementary mouse models of colitis: either chemically (dextran sulfate sodium) or with Citrobacter rodentium infection.
  
  
  METHODS
  After sacrifice, the tongue, buccal mucosa, saliva, colon, and stool samples were collected for analyses. Denaturing gradient gel electrophoresis was performed to assess bacterial 16S rRNA gene profiles. Relative changes were determined using quantitative polymerase chain reaction analysis for the phyla Bacteroidetes, Firmicutes, Spirochetes, and Actinobacteria, classes Gammaproteobacteria and Betaproteobacteria, and the genera Bacillus and Lactobacillus. These groups represent over 99% of the oral microbiota of healthy C57BL/6 mice.
  
  
  RESULTS
  Both models of colitis changed the oral microbiome, with the buccal microbiome being the most resistant to alterations in composition (maximum 1.8% change, vs tongue maximum 2.5% change, and saliva which demonstrated up to 7.2% total changes in microbiota composition). Changes in the oral microbiota were greater after dextran sulfate sodium challenge, compared with C. rodentium-induced colitis. Using cluster analysis, tongue and buccal mucosal microbiota composition changed ∼ 5%, saliva ∼ 35%, while stool changed ∼ 10%.
  
  
  CONCLUSIONS
  These findings indicate that dysbiosis observed in murine models of colitis is associated with changes in the composition of bacteria present in the oral cavity and in saliva. Such changes in the oral microbiota could be relevant to the etiology and management of oral mucosal pathologies observed in IBD patients.
authors.affiliation: Cell Biology Program, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Oral Pathology and Oral Radiology, Institute of Dentistry, University of Turku, Turku, Finland.
authors.forename: Jaana
authors.initials: J
authors.lastname: Rautava
authors.forename: Lee J
authors.initials: LJ
authors.lastname: Pinnell
authors.forename: Linda
authors.initials: L
authors.lastname: Vong
authors.forename: Nadia
authors.initials: N
authors.lastname: Akseer
authors.forename: Amit
authors.initials: A
authors.lastname: Assa
authors.forename: Philip M
authors.initials: PM
authors.lastname: Sherman
mesh_terms: D000818:Animals; D044082:Citrobacter rodentium / Q000235:genetics; D003092:Colitis / Q000139:chemically induced / Q000382:microbiology*; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D064806:Dysbiosis; D004756:Enterobacteriaceae Infections; D005243:Feces / Q000382:microbiology; D054884:Host-Pathogen Interactions; D008297:Male; D008810:Mice, Inbred C57BL; D064307:Microbiota / Q000502:physiology; D009055:Mouth / Q000382:microbiology*; D009061:Mouth Mucosa / Q000382:microbiology*; D012336:RNA, Ribosomal, 16S; D012463:Saliva / Q000382:microbiology; D014059:Tongue / Q000382:microbiology
chemical_list: D012336:RNA, Ribosomal, 16S; D016264:Dextran Sulfate
keywords: Citrobacter rodentium; Crohn's disease; inflammatory bowel disease; microbiome; ulcerative colitis