title: Gut microbiota and development of atopic eczema in 3 European birth cohorts.
abstract: BACKGROUND
  Stimulation of the immune system by gut microbes might prevent allergy development.
  
  
  OBJECTIVE
  The present study examined the hypothesis that sensitization to food allergens and atopic eczema are influenced by the infantile intestinal colonization pattern.
  
  
  METHODS
  Infants were recruited perinatally in Göteborg (n = 116), London (n = 108), and Rome (n = 100). Commensal bacteria were identified to the genus or species level in rectal (3 days) and quantitative stool cultures (7, 14, and 28 days and 2, 6, and 12 months of age). At 18 months of age, atopic eczema and total and food-specific IgE levels were assessed. These outcomes were modeled in relation to time to colonization with 11 bacterial groups and to ratios of strict anaerobic to facultative anaerobic bacteria and gram-positive to gram-negative bacteria at certain time points. Study center, mode of delivery, parity, and infant diet were included as covariates.
  
  
  RESULTS
  Neither atopic eczema nor food-specific IgE by 18 months of age were associated with time of acquisition of any particular bacterial group. Cesarean section delayed colonization by Escherichia coli and Bacteroides and Bifidobacterium species, giving way to, for example, Clostridium species. Lack of older siblings was associated with earlier colonization by Clostridium species and lower strict anaerobic/facultative anaerobic ratio at 12 months.
  
  
  CONCLUSIONS
  This study does not support the hypothesis that sensitization to foods or atopic eczema in European infants in early life is associated with lack of any particular culturable intestinal commensal bacteria.
  
  
  CONCLUSIONS
  The nature of the microbial stimulus required for protection from allergy remains to be identified.
authors.affiliation: Department of Clinical Bacteriology, St George's, University of London, London, United Kingdom. ingegerd.adlerberth@microbio.gu.se
authors.forename: Ingegerd
authors.initials: I
authors.lastname: Adlerberth
authors.forename: David P
authors.initials: DP
authors.lastname: Strachan
authors.forename: Paolo M
authors.initials: PM
authors.lastname: Matricardi
authors.forename: Siv
authors.initials: S
authors.lastname: Ahrné
authors.forename: Lia
authors.initials: L
authors.lastname: Orfei
authors.forename: Nils
authors.initials: N
authors.lastname: Aberg
authors.forename: Michael R
authors.initials: MR
authors.lastname: Perkin
authors.forename: Salvatore
authors.initials: S
authors.lastname: Tripodi
authors.forename: Bill
authors.initials: B
authors.lastname: Hesselmar
authors.forename: Robert
authors.initials: R
authors.lastname: Saalman
authors.forename: Anthony R
authors.initials: AR
authors.lastname: Coates
authors.forename: Carmen L
authors.initials: CL
authors.lastname: Bonanno
authors.forename: Valentina
authors.initials: V
authors.lastname: Panetta
authors.forename: Agnes E
authors.initials: AE
authors.lastname: Wold
mesh_terms: D000375:Aging / Q000276:immunology; D000485:Allergens / Q000276:immunology; D001439:Bacteroides / Q000254:growth & development; D001644:Bifidobacterium / Q000254:growth & development; D002585:Cesarean Section; D003013:Clostridium / Q000254:growth & development; D015331:Cohort Studies; D015169:Colony Count, Microbial; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000382:microbiology*; D004926:Escherichia coli / Q000254:growth & development; D005060:Europe; D005243:Feces / Q000382:microbiology; D005260:Female; D005512:Food Hypersensitivity / Q000097:blood / Q000276:immunology* / Q000382:microbiology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007231:Infant, Newborn; D008019:Life Style; D008137:Longitudinal Studies; D008297:Male; D012007:Rectum / Q000382:microbiology*; D012307:Risk Factors
chemical_list: D000485:Allergens; D007073:Immunoglobulin E