title: Gut microbiota composition and development of atopic manifestations in infancy: the KOALA Birth Cohort Study.
abstract: OBJECTIVE
  Perturbations in intestinal microbiota composition due to lifestyle changes may be involved in the development of atopic diseases. We examined gut microbiota composition in early infancy and the subsequent development of atopic manifestations and sensitisation.
  
  
  METHODS
  The faeces of 957 infants aged 1 month and participating in the KOALA Birth Cohort Study were analysed using quantitative real-time PCR. Information on atopic symptoms (eczema, wheeze) and potential confounders was acquired through repeated questionnaires. Total and specific IgE were measured in venous blood samples collected during home visits when the infant was 2 years old. During these home visits a clinical diagnosis of atopic dermatitis was made according to the UK-Working Party criteria.
  
  
  RESULTS
  The presence of Escherichia coli was associated with a higher risk of developing eczema (OR(adj) = 1.87; 95% CI 1.15 to 3.04), this risk being increased with increasing numbers of E coli (p(for trend) = 0.016). Infants colonised with Clostridium difficile were at higher risk of developing eczema (OR(adj) = 1.40; 95% CI 1.02 to 1.91), recurrent wheeze (OR(adj) = 1.75; 95% CI 1.09 to 2.80) and allergic sensitisation (OR(adj) = 1.54; 95% CI 1.02 to 2.31). Furthermore, the presence of C difficile was also associated with a higher risk of a diagnosis of atopic dermatitis during the home visit (OR(adj) = 1.73; 95% CI 1.08 to 2.78).
  
  
  CONCLUSIONS
  This study demonstrates that differences in gut microbiota composition precede the development of atopy. Since E coli was only associated with eczema and C difficile was associated with all atopic outcomes, the underlying mechanisms explaining these association may be different.
authors.affiliation: Department of Epidemiology, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD Maastricht, the Netherlands. j.penders@epid.unimaas.nl
authors.forename: John
authors.initials: J
authors.lastname: Penders
authors.forename: Carel
authors.initials: C
authors.lastname: Thijs
authors.forename: Piet A
authors.initials: PA
authors.lastname: van den Brandt
authors.forename: Ischa
authors.initials: I
authors.lastname: Kummeling
authors.forename: Bianca
authors.initials: B
authors.lastname: Snijders
authors.forename: Foekje
authors.initials: F
authors.lastname: Stelma
authors.forename: Hanne
authors.initials: H
authors.lastname: Adams
authors.forename: Ronald
authors.initials: R
authors.lastname: van Ree
authors.forename: Ellen E
authors.initials: EE
authors.lastname: Stobberingh
mesh_terms: D001419:Bacteria / Q000302:isolation & purification*; D016360:Clostridioides difficile / Q000302:isolation & purification; D004269:DNA, Bacterial / Q000302:isolation & purification; D003876:Dermatitis, Atopic / Q000276:immunology / Q000382:microbiology; D004926:Escherichia coli / Q000302:isolation & purification; D005243:Feces / Q000382:microbiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology / Q000382:microbiology*; D007073:Immunoglobulin E / Q000097:blood; D007223:Infant; D008297:Male; D016133:Polymerase Chain Reaction / Q000379:methods; D011446:Prospective Studies; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000382:microbiology; D012135:Respiratory Sounds / Q000276:immunology
chemical_list: D004269:DNA, Bacterial; D007073:Immunoglobulin E