title: Oral application of bacterial lysate in infancy decreases the risk of atopic dermatitis in children with 1 atopic parent in a randomized, placebo-controlled trial.
abstract: BACKGROUND
  Lower prevalence of atopy was found in children with continuous exposure to livestock and thus to microbial compounds. In animal models exposure to endotoxin (LPS) decreases allergic sensitization and airway inflammation.
  
  
  OBJECTIVE
  We sought to evaluate the effect of orally applied bacterial lysate in infancy on the prevalence of atopic dermatitis (AD) after the treatment phase at 7 months of age.
  
  
  METHODS
  This randomized, placebo-controlled trial included 606 newborns with at least single heredity for atopy. From week 5 until the end of month 7, infants were treated orally with bacterial lysate containing heat-killed gram-negative Escherichia coli Symbio and gram-positive Enterococcus faecalis Symbio or its placebo. Children were followed until 3 years of age.
  
  
  RESULTS
  There was no difference in the primary outcome between the active and placebo groups in the total study group. AD prevalence was significantly reduced at the end of the intervention phase (31 weeks of age) in the subgroup of infants with single heredity for atopy (relative risk, 0.52; 95% CI, 0.3-0.9). Ten percent (15/154) of infants in the active group had AD compared with 19% (27/145, P = .030) in the placebo group. This was more pronounced in the group of infants with paternal heredity for atopy (11% vs 32%, P = .004; relative risk, 0.34; 95% CI, 0.2-0.7).
  
  
  CONCLUSIONS
  Feeding of bacterial lysate might have prevented the development of AD, especially in children with paternal atopy, possibly indicating a preventive property only in subjects with a limited risk for atopy.
authors.affiliation: Department of Pediatric Pneumology and Immunology, Charité Medical University Berlin, Berlin, Germany. susanne.lau@charite.de
authors.forename: Susanne
authors.initials: S
authors.lastname: Lau
authors.forename: Kerstin
authors.initials: K
authors.lastname: Gerhold
authors.forename: Kurt
authors.initials: K
authors.lastname: Zimmermann
authors.forename: Charlotte W
authors.initials: CW
authors.lastname: Ockeloen
authors.forename: Siri
authors.initials: S
authors.lastname: Rossberg
authors.forename: Petra
authors.initials: P
authors.lastname: Wagner
authors.forename: Claudia
authors.initials: C
authors.lastname: Sulser
authors.forename: Rita
authors.initials: R
authors.lastname: Bunikowski
authors.forename: Imke
authors.initials: I
authors.lastname: Witt
authors.forename: Juliane
authors.initials: J
authors.lastname: Wauer
authors.forename: John
authors.initials: J
authors.lastname: Beschorner
authors.forename: Georg
authors.initials: G
authors.lastname: Menke
authors.forename: Eckard
authors.initials: E
authors.lastname: Hamelmann
authors.forename: Ulrich
authors.initials: U
authors.lastname: Wahn
mesh_terms: D000284:Administration, Oral; D001419:Bacteria / Q000276:immunology*; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000453:epidemiology / Q000276:immunology / Q000517:prevention & control*; D003888:Desensitization, Immunologic; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007223:Infant; D008297:Male; D010290:Parents; D015995:Prevalence; D012306:Risk
chemical_list: D007073:Immunoglobulin E