title: Reduced diversity in the early fecal microbiota of infants with atopic eczema.
abstract: BACKGROUND
  It might be that early intestinal colonization by bacteria in westernized infants fails to give rise to sufficient immune stimulation to support maturation of regulatory immune mechanisms.
  
  
  OBJECTIVE
  The purpose of the present study was to characterize the very early infantile microbiota by using a culture-independent approach and to relate the colonization pattern to development of atopic eczema in the first 18 months of life.
  
  
  METHODS
  Fecal samples were collected from 35 infants at 1 week of age. Twenty infants were healthy, and 15 infants were given diagnoses of atopic eczema at the age of 18 months. The fecal microbiota of the infants was compared by means of terminal restriction fragment length polymorphism (T-RFLP) and temporal temperature gradient gel electrophoresis (TTGE) analysis of amplified 16S rRNA genes.
  
  
  RESULTS
  By means of T-RFLP analysis, the median number of peaks, Shannon-Wiener index, and Simpson index of diversity were significantly less for infants with atopic eczema than for infants remaining healthy in the whole group and for the Swedish infants when AluI was used for digestion. The same was found when TTGE patterns were compared. In addition, TTGE analysis showed significantly less bands and lower diversity indices for the British atopic infants compared with those of the control subjects.
  
  
  CONCLUSIONS
  There is a reduced diversity in the early fecal microbiota of infants with atopic eczema during the first 18 months of life.
authors.affiliation: Department of Food Technology, Engineering and Nutrition, Lund University, Lund, Sweden.
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.forename: Caroline
authors.initials: C
authors.lastname: Karlsson
authors.forename: Crister
authors.initials: C
authors.lastname: Olsson
authors.forename: Ingegerd
authors.initials: I
authors.lastname: Adlerberth
authors.forename: Agnes E
authors.initials: AE
authors.lastname: Wold
authors.forename: David P
authors.initials: DP
authors.lastname: Strachan
authors.forename: Paolo M
authors.initials: PM
authors.lastname: Martricardi
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: Anthony R
authors.initials: AR
authors.lastname: Coates
authors.forename: Bill
authors.initials: B
authors.lastname: Hesselmar
authors.forename: Robert
authors.initials: R
authors.lastname: Saalman
authors.forename: Göran
authors.initials: G
authors.lastname: Molin
authors.forename: Siv
authors.initials: S
authors.lastname: Ahrné
mesh_terms: D001419:Bacteria / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification; D004269:DNA, Bacterial / Q000032:analysis / Q000302:isolation & purification; D003876:Dermatitis, Atopic / Q000276:immunology / Q000382:microbiology*; D004587:Electrophoresis, Agar Gel; D005243:Feces / Q000382:microbiology*; D014644:Genetic Variation; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D012150:Polymorphism, Restriction Fragment Length; D012336:RNA, Ribosomal, 16S / Q000235:genetics
chemical_list: D004269:DNA, Bacterial; D012336:RNA, Ribosomal, 16S