title: Smokers with active Crohn's disease have a clinically relevant dysbiosis of the gastrointestinal microbiota.
abstract: BACKGROUND
  Patients with Crohn's disease (CD) have an intestinal dysbiosis with components of the microbiota exerting differential immune effects. Smoking is associated with an increased incidence of CD, more frequent relapse, and greater burden of surgery. This study aimed to investigate the association between smoking and the intestinal microbiota in patients with active CD.
  
  
  METHODS
  Patients with active CD (n = 103) and healthy controls (n = 66) were recruited and demographic and clinical data recorded including current smoking behavior. Fecal samples were collected and analyzed by fluorescent in situ hybridization using probes targeting 16S rRNA of bacteria previously shown to be altered in active CD (bifidobacteria, bacteroides, Clostridium coccoides-Eubacterium rectale, Escherichia coli, and Faecalibacterium prausnitzii).
  
  
  RESULTS
  In total, 29/101 (29%) patients with CD and 8/58 (14%) controls were current smokers (P = 0.032). Following multivariate analysis, smoking was found to have a significant and independent effect on the microbiota of patients with CD, with higher Bacteroides-Prevotella in smokers (38.4%) compared with nonsmokers (28.1%) (F((1,93)) = 12.6, P = 0.001). Healthy controls who smoked also had higher Bacteroides-Prevotella (34.8%) than nonsmokers (24.1%) (F((1,55)) = 4.5, P = 0.038). In the pooled multivariate analysis, patients with CD had higher bifidobacteria (F((1,156)) = 30.5, P < 0.001), higher Bacteroides-Prevotella (F((1,156)) = 6.5, P = 0.012), and lower F. prausnitzii (F((1,156)) = 3.8, P = 0.052) compared with healthy controls.
  
  
  CONCLUSIONS
  Smokers have luminal microbiota that consist of significantly higher bacteroides. Investigation of whether this is one mechanism through which the negative effects of smoking on CD are mediated is warranted.
authors.affiliation: King's College London, School of Medicine, Diabetes and Nutritional Sciences Division, London, UK.
authors.forename: Jane L
authors.initials: JL
authors.lastname: Benjamin
authors.forename: Charlotte R H
authors.initials: CR
authors.lastname: Hedin
authors.forename: Andreas
authors.initials: A
authors.lastname: Koutsoumpas
authors.forename: Siew C
authors.initials: SC
authors.lastname: Ng
authors.forename: Neil E
authors.initials: NE
authors.lastname: McCarthy
authors.forename: Natalie J
authors.initials: NJ
authors.lastname: Prescott
authors.forename: Pedro
authors.initials: P
authors.lastname: Pessoa-Lopes
authors.forename: Christopher G
authors.initials: CG
authors.lastname: Mathew
authors.forename: Jeremy
authors.initials: J
authors.lastname: Sanderson
authors.forename: Ailsa L
authors.initials: AL
authors.lastname: Hart
authors.forename: Michael A
authors.initials: MA
authors.lastname: Kamm
authors.forename: Stella C
authors.initials: SC
authors.lastname: Knight
authors.forename: Alastair
authors.initials: A
authors.lastname: Forbes
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Stagg
authors.forename: James O
authors.initials: JO
authors.lastname: Lindsay
authors.forename: Kevin
authors.initials: K
authors.lastname: Whelan
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D015169:Colony Count, Microbial; D003424:Crohn Disease / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology*; D004269:DNA, Bacterial / Q000235:genetics; D005243:Feces / Q000382:microbiology; D005260:Female; D041981:Gastrointestinal Tract / Q000187:drug effects / Q000382:microbiology* / Q000473:pathology*; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D054892:Metagenome; D011446:Prospective Studies; D012907:Smoking / Q000009:adverse effects*
chemical_list: D004269:DNA, Bacterial