title: A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes.
abstract: OBJECTIVE
  The composition of the gastrointestinal microbiota is thought to have an important role in the etiology of inflammatory bowel diseases (IBDs) such as Crohn's disease (CD) and ulcerative colitis (UC). Interindividual variation and an inability to detect less abundant bacteria have made it difficult to correlate specific bacteria with disease.
  
  
  METHODS
  We used 454 pyrotag sequencing to determine the compositions of microbial communities in feces samples collected from a cohort of 40 twin pairs who were concordant or discordant for CD or UC, and in mucosal samples from a subset of the cohort. The cohort primarily comprised patients who were in remission, but also some with active disease.
  
  
  RESULTS
  The profiles of the microbial community differed with disease phenotypes; relative amounts of bacterial populations correlated with IBD phenotypes. The microbial compositions of individuals with CD differed from those of healthy individuals, but were similar between healthy individuals and individuals with UC. Profiles from individuals with CD that predominantly involved the ileum differed from those with CD that predominantly involved the colon; several bacterial populations increased or decreased with disease type. Changes specific to patients with ileal CD included the disappearance of core bacteria, such as Faecalibacterium and Roseburia, and increased amounts of Enterobacteriaceae and Ruminococcus gnavus.
  
  
  CONCLUSIONS
  Bacterial populations differ in abundance among individuals with different phenotypes of CD. Specific species of bacteria are associated with ileal CD; further studies should investigate their role in pathogenesis.
authors.affiliation: Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden.
authors.forename: Ben P
authors.initials: BP
authors.lastname: Willing
authors.forename: Johan
authors.initials: J
authors.lastname: Dicksved
authors.forename: Jonas
authors.initials: J
authors.lastname: Halfvarson
authors.forename: Anders F
authors.initials: AF
authors.lastname: Andersson
authors.forename: Marianna
authors.initials: M
authors.lastname: Lucio
authors.forename: Zongli
authors.initials: Z
authors.lastname: Zheng
authors.forename: Gunnar
authors.initials: G
authors.lastname: Järnerot
authors.forename: Curt
authors.initials: C
authors.lastname: Tysk
authors.forename: Janet K
authors.initials: JK
authors.lastname: Jansson
authors.forename: Lars
authors.initials: L
authors.lastname: Engstrand
mesh_terms: D000328:Adult; D000368:Aged; D001419:Bacteria / Q000145:classification / Q000235:genetics*; D001706:Biopsy; D003093:Colitis, Ulcerative / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D003106:Colon / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D003424:Crohn Disease / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D005243:Feces / Q000382:microbiology; D005798:Genes, Bacterial / Q000235:genetics; D006801:Humans; D007082:Ileum / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D054892:Metagenome / Q000235:genetics* / Q000276:immunology*; D008875:Middle Aged; D010641:Phenotype; D012335:RNA, Ribosomal / Q000235:genetics; D017422:Sequence Analysis, DNA / Q000379:methods; D014429:Twins, Dizygotic / Q000235:genetics / Q000276:immunology; D014430:Twins, Monozygotic / Q000235:genetics / Q000276:immunology
chemical_list: D012335:RNA, Ribosomal